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Insulin-like growth factor 2 targets IGF1R signaling transduction to facilitate metastasis and imatinib resistance in gastrointestinal stromal tumors
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作者 De-Gang Li Jia-Peng Jiang +4 位作者 Fan-Ye Chen Wei Wu Jun Fu Gong-He Wang Yu-Bo Li 《World Journal of Gastrointestinal Oncology》 SCIE 2024年第8期3585-3599,共15页
BACKGROUND Gastrointestinal stromal tumors(GISTs)are typical gastrointestinal tract neoplasms.Imatinib is the first-line therapy for GIST patients.Drug resistance limits the long-term effectiveness of imatinib.The reg... BACKGROUND Gastrointestinal stromal tumors(GISTs)are typical gastrointestinal tract neoplasms.Imatinib is the first-line therapy for GIST patients.Drug resistance limits the long-term effectiveness of imatinib.The regulatory effect of insulin-like growth factor 2(IGF2)has been confirmed in various cancers and is related to resistance to chemotherapy and a worse prognosis.AIM To further investigate the mechanism of IGF2 specific to GISTs.METHODS IGF2 was screened and analyzed using Gene Expression Omnibus(GEO:GSE225819)data.After IGF2 knockdown or overexpression by transfection,the phenotypes(proliferation,migration,invasion,apoptosis)of GIST cells were characterized by cell counting kit 8,Transwell,and flow cytometry assays.We used western blotting to evaluate pathway-associated and epithelial-mesenchymal transition(EMT)-associated proteins.We injected transfected cells into nude mice to establish a tumor xenograft model and observed the occurrence and metastasis of GIST.RESULTS Data from the GEO indicated that IGF2 expression is high in GISTs,associated with liver metastasis,and closely related to drug resistance.GIST cells with high expression of IGF2 had increased proliferation and migration,invasiveness and EMT.Knockdown of IGF2 significantly inhibited those activities.In addition,OEIGF2 promoted GIST metastasis in vivo in nude mice.IGF2 activated IGF1R signaling in GIST cells,and IGF2/IGF1R-mediated glycolysis was required for GIST with liver metastasis.GIST cells with IGF2 knockdown were sensitive to imatinib treatment when IGF2 overexpression significantly raised imatinib resistance.Moreover,2-deoxy-D-glucose(a glycolysis inhibitor)treatment reversed IGF2 overexpressionmediated imatinib resistance in GISTs.CONCLUSION IGF2 targeting of IGF1R signaling inhibited metastasis and decreased imatinib resistance by driving glycolysis in GISTs. 展开更多
关键词 insulin-like growth factor 2 Gastrointestinal stromal tumors IGF1R GLYCOLYSIS Imatinib resistance
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Single Nucleotide Polymorphism Analysis on 5' Regulatory Region of Goose Insulin-like Growth FactorⅠGene
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作者 杜晓东 张绍胜 +3 位作者 姜润深 夏生林 耿照玉 袁绍友 《Animal Husbandry and Feed Science》 CAS 2009年第2期13-14,42,共3页
[ Objedive] This study was aimed to determine the single nucleotide polymorphisms (SNPs) of IGF-I gene in two breeds, Wanxi white goose and Langde goose. [ Method] Two pair of primers was designed based on chicken a... [ Objedive] This study was aimed to determine the single nucleotide polymorphisms (SNPs) of IGF-I gene in two breeds, Wanxi white goose and Langde goose. [ Method] Two pair of primers was designed based on chicken and porcine genomic sequence to amplify the 5' regulatory region of IGF-I, and the sequence was determined and analyzed. [ Result] A total of four SNPs were identified in this region by PCR-SSCP meth- od, that is, A to T at 26 nt, A to G at 215 nt, A to G at 314 nt, and A to T at 325 nt. [ Conclusioa] The two breeds ,wanxi white geese and Langde geese, agree with Hardy-weinberg equilibrium with respect to these SNPS. 展开更多
关键词 GOOSE insulin-like growth factorlgene Single nucleotide polymorphisms
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Insulin-like growth factor-1 induces lymphangiogenesis and facilitates lymphatic metastasis in colorectal cancer 被引量:12
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作者 Zhen-Jun Li Xiao-Jiang Ying +6 位作者 Hong-Liang Chen Ping-Jiang Ye Zhi-Liang Chen Gang Li Hua-Feng Jiang Jiang Liu Shu-Zhen Zhou 《World Journal of Gastroenterology》 SCIE CAS 2013年第43期7788-7794,共7页
AIM:To investigate the expression of insulin-like growth factor-1(IGF-1)/insulin-like growth factor-1 receptor(IGF-1R)in colorectal cancer(CRC)tissues and to analyze their correlation with lymphangiogenesis and lympha... AIM:To investigate the expression of insulin-like growth factor-1(IGF-1)/insulin-like growth factor-1 receptor(IGF-1R)in colorectal cancer(CRC)tissues and to analyze their correlation with lymphangiogenesis and lymphatic metastasis.METHODS:Immunohistochemistry was used to evaluate IGF-1 and IGF-1R expression and lymphatic vessel density(LVD)in 40 CRC specimens.The correlation between IGF-1/IGF-1R and LVD was investigated.Effects of IGF-1 on migration and invasion of CRC cells were examined using transwell chamber assays.A LoVo cell xenograft model was established to further detect the role of IGF-1 in CRC lymphangiogenesis in vivo. RESULTS:Elevated IGF-1 and IGF-1R expression in CRC tissues was correlated with lymph node metastasis(r=0.715 and 0.569,respectively,P<0.05)and tumor TNM stage(r=0.731 and 0.609,P<0.05).A higher LVD was also found in CRC tissues and was correlated with lymphatic metastasis(r=0.405,P<0.05).A positive correlation was found between LVD and IGF-1R expression(r=0.437,P<0.05).Transwell assays revealed that IGF-1 increased the migration and invasion of CRC cells.In vivo mouse studies showed that IGF-1 also increased LVD in LoVo cell xenografts.CONCLUSION:IGF-1/IGF-1R signaling induces tumorassociated lymphangiogenesis and contributes to lymphatic metastasis of CRC. 展开更多
关键词 Colorectal cancer insulin-like growth factor-1 insulin-like growth factor-1 receptor LYMPHANGIOGENESIS Lymphatic metastasis
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Targeting the insulin-like growth factor pathway in hepatocellular carcinoma 被引量:11
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作者 Mónica Enguita-Germán Puri Fortes 《World Journal of Hepatology》 CAS 2014年第10期716-737,共22页
Hepatocellular carcinoma(HCC) is the third leading cause of cancer-related deaths worldwide. Only 30%-40% of the patients with HCC are eligible for curative treatments, which include surgical resection as the first op... Hepatocellular carcinoma(HCC) is the third leading cause of cancer-related deaths worldwide. Only 30%-40% of the patients with HCC are eligible for curative treatments, which include surgical resection as the first option, liver transplantation and percutaneous ablation. Unfortunately, there is a high frequency of tumor recurrence after surgical resection and most HCC seem resistant to conventional chemotherapy and radiotherapy. Sorafenib, a multi-tyrosine kinase inhibitor, is the only chemotherapeutic option for patients with advanced hepatocellular carcinoma. Patients treated with Sorafenib have a significant increase in overall survival of about three months. Therefore, there is an urgent need to develop alternative treatments. Due to its role in cell growth and development, the insulin-like growth factor system is commonly deregulated in many cancers. Indeed, the insulin-like growth factor(IGF) axis has recently emerged as a potential target for hepatocellular carcinoma treatment. To this aim, several inhibitors of the pathway have been developed suchas monoclonal antibodies, small molecules, antisense oligonucleotides or small interfering RNAs. However recent studies suggest that, unlike most tumors, HCC development requires increased signaling through insulin growth factor Ⅱ rather than insulin growth factor Ⅰ. This may have great implications in the future treatment of HCC. This review summarizes the role of the IGF axis in liver carcinogenesis and the current status of the strategies designed to target the IGF-Ⅰ signaling pathway for hepatocellular carcinoma treatment. 展开更多
关键词 HEPATOCELLULAR carcinoma Insulin Insulinlike growth FACTOR Insulinlike growth FACTOR receptor THERAPY TYROSINE KINASE inhibitor Antibody THERAPY
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Expression of insulin-like growth factor Ⅱ and its receptor in liver cells of chronic liver diseases 被引量:21
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作者 YANG Dong Hua 1, XIU Chong 1, YANG Bo 1, GU Jian Ren 2, QIAN Lian Fang 2 and QU Shu Ming 2 《World Journal of Gastroenterology》 SCIE CAS CSCD 1997年第2期60-61,共2页
AIM To clarify the relationship between the Insulin like growth factor Ⅱ (IGF Ⅱ), IGF Ⅱ receptor and chronic liver diseases and to provide evidences for basic and clinical researches for exploring the potential... AIM To clarify the relationship between the Insulin like growth factor Ⅱ (IGF Ⅱ), IGF Ⅱ receptor and chronic liver diseases and to provide evidences for basic and clinical researches for exploring the potential mechanisms of human hepatocellular carcinoma (HCC). METHODS The poly (A)+ mRNA translation of IGF Ⅱ and IGF Ⅱ receptor in dysplasia liver cell (DLC n =10), liver cirrhosis (LC n =9) and chronic active hepatitis (CAH n =9) were analyzed with RNA gel electrophoresis, Northern blot and hybridization using human IGF Ⅱ and IGF Ⅱ receptor DNA probes labelled with 32 P through Nick translation and autoradiography. RESULTS The overexpression of IGF Ⅱ in DLC (10/10, 100%) was apparently higher than that in CAH (3/9, 33%) and LC (3/9, 33%), ( P <0 01). The overexpression of IGF Ⅱ receptor in DLC (7/10, 70%) was significantly higher than that in CAH (2/9, 22%) and LC (3/9, 33%), respectively. The data of HBV infection from different chronic liver diseases were analyzed. CONCLUSION The overexpression of IGF Ⅱ and IGF Ⅱ receptor in DLC was related to the preceeding of malignant phenotype of hepatocyte, which provided a diagnostic value for early detection of hepatocellular carcinoma (HCC). Persistent HBV infection is strongly associated with abnormal activation of IGF Ⅱ and IGF Ⅱ receptor, which might indicate a stimulating mechanism of autocrine or paracrine growth involved in live cell carcinogenesis. 展开更多
关键词 insulin like growth FACTOR receptors somato medin carcinoma hepatocellular hepatitis LIVER NEOPLASMS LIVER cirrhosis LIVER DISEASES
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Expression of insulin-like growth factor Ⅱ and its receptor in hepatocellular carcinogenesis 被引量:24
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作者 Zi Rong Fan Dong Hua Yang +2 位作者 Jun Cui Han Rong Qin Chun Chi Huang Department of Gastroenterology, Zhujiang Hospital. The First Military Medical University, Guangzhou 510282.Guangdong Province. China 《World Journal of Gastroenterology》 SCIE CAS CSCD 2001年第2期285-288,共4页
INTRODUCTIONInsulin-like growth factor Ⅱ(IGF-Ⅱ) is a mitogenic peptide of 74 kD and is mostly synthesized in fetal liver tissue .IGF-Ⅱ is believed to play an important role in fetal growth and development and is in... INTRODUCTIONInsulin-like growth factor Ⅱ(IGF-Ⅱ) is a mitogenic peptide of 74 kD and is mostly synthesized in fetal liver tissue .IGF-Ⅱ is believed to play an important role in fetal growth and development and is involved in cellular proliferation and differentiation[1-5]. Recently ,several researchers have reported increased expression of the IGF-Ⅱgene in human hepatocellular carcinoma (HCC) and adjacent non-cancerous liver tissues [6-10]. 展开更多
关键词 liver neoplasms/pathology insulin-like growth factor Ⅱ/biosynthesis receptors somatomedin/biosynthesis RNA messenger/biosynthesis in situ hybridization hepatitis chronic/pathology
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A candidate targeting molecule of insulin-like growth factor-Ⅰ receptor for gastrointestinal cancers 被引量:14
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作者 Yasushi Adachi Hiroyuki Yamamoto +4 位作者 Hirokazu Ohashi Takao Endo David P Carbone Kohzoh Imai Yasuhisa Shinomura 《World Journal of Gastroenterology》 SCIE CAS CSCD 2010年第46期5779-5789,共11页
Advances in molecular research in cancer have brought new therapeutic strategies into clinical usage.One new group of targets is tyrosine kinase receptors,which can be treated by several strategies,including small mol... Advances in molecular research in cancer have brought new therapeutic strategies into clinical usage.One new group of targets is tyrosine kinase receptors,which can be treated by several strategies,including small molecule tyrosine kinase inhibitors(TKIs) and monoclonal antibodies(mAbs).Aberrant activation of growth factors/receptors and their signal pathways are required for malignant transformation and progression in gastrointestinal(GI) carcinomas.The concept of targeting specif ic carcinogenic receptors has been validated by successful clinical application of many new drugs.Type I insulin-like growth factor(IGF) receptor(IGF-IR) signaling potently stimulates tumor progression and cellular differentiation,and is a promising new molecular target in human malignancies.In this review,we focus on this promising therapeutic target,IGF-IR.The IGF/IGF-IR axis is an important modifier of tumor cell proliferation,survival,growth,and treatment sensitivity in many malignant diseases,including human GI cancers.Preclinical studies demonstrated that downregulation of IGF-IR signals reversed the neoplastic phenotype and sensitized cells to anticancer treatments.These results were mainly obtained through our strategy of adenoviruses expressing dominant negative IGF-IR(IGF-IR/dn) against gastrointestinal cancers,including esophagus,stomach,colon,and pancreas.We also summarize a variety of strategies to interrupt the IGFs/IGF-IR axis and their preclinical experiences.Several mAbs and TKIs targeting IGF-IR have entered clinical trials,and early results have suggested that these agents have generally acceptable safety profiles as single agents.We summarize the advantages and disadvantages of each strategy and discuss the merits/demerits of dual targeting of IGF-IR and other growth factor receptors,including Her2 and the insulin receptor,as well as other alternatives and possible drug combinations.Thus,IGF-IR might be a candidate for a molecular therapeutic target in human GI carcinomas. 展开更多
关键词 DOMINANT negative GASTROINTESTINAL cancer Insulin like growth FACTOR-I RECEPTOR MONOCLONAL anti-body TYROSINE kinase inhibitor
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Insulin-like growth factor-I receptor in proliferation and motility of pancreatic cancer 被引量:12
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作者 Minoru Tomizawa Fuminobu Shinozaki +3 位作者 Takao Sugiyama Shigenori Yamamoto Makoto Sueishi Takanobu Yoshida 《World Journal of Gastroenterology》 SCIE CAS CSCD 2010年第15期1854-1858,共5页
AIM:To develop a molecular therapy for pancreatic cancer, the insulin-like growth factor-I (IGF-I) signaling pathway was analyzed.METHODS: Pancreatic cancer cell lines (MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 a... AIM:To develop a molecular therapy for pancreatic cancer, the insulin-like growth factor-I (IGF-I) signaling pathway was analyzed.METHODS: Pancreatic cancer cell lines (MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 and KP-4) were cultured in media with 10 mL/L fetal bovine serum. Western blotting analysis was performed to clarify the expression of IGF-I receptor (IGF-IR). Picropodophyllin (PPP), a specific inhibitor of IGF-IR, LY294002, a specific inhibitor of phosphatidylinositol3 kinase (PI3K), and PD98059, a specific inhibitor of mitogen-activated protein kinase, were added to the media. After 72 h, a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium inner salt (MTS) assay was performed to analyze cell proliferation. A wound assay was performed to analyze cell motility with hematoxylin and eosin (HE) staining 48 h after addition of each inhibitor. RESULTS: All cell lines clearly expressed not only IGF-IR but also phosphorylated IGF-IR. PPP significantly suppressed proliferation of MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 and KP-4 cells to 36.9% ± 2.4% (mean ± SD), 30.9% ± 5.5%, 23.8% ± 3.9%, 37.1% ± 5.3%, 10.4% ± 4.5%, 52.5% ± 4.5% and 22.6% ± 0.4%, at 2 μmol/L, respectively (P < 0.05). LY294002 significantly suppressed proliferation of MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 and KP-4 cells to 44.4% ± 7.6%, 32.9% ± 8.2%, 53.9% ± 8.0%, 52.8% ± 4.0%, 32.3% ± 4.2%, 51.8% ± 4.5%, and 30.6% ± 9.4%, at 50 μmol/L, respectively (P < 0.05). PD98059 did not significantly suppress cell proliferation. PPP at 2 μmol/L suppressed motility of MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 and KP-4 cells to 3.0% ± 0.2%, 0%, 0%, 2.0% ± 0.1%, 5.0% ± 0.2%, 3.0% ± 0.1%, and 5.0% ± 0.2%, respectively (P < 0.05). LY294002 at 50 μmol/L suppressed motility of MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 and KP-4 to 3.0% ± 0.2%, 0%, 3.0% ± 0.2%, 0%, 0%, 0% and 3% ± 0.1%, respectively (P < 0.05). PD980509 at 20 μmol/L did not suppress motility. Cells were observed by microscopy to analyze the morphological changes induced by the inhibitors. Cells in medium treated with 2 μmol/L PPP or 50 μmol/L LY294002 had pyknotic nuclei, whereas those in medium with 20 μmol/L PD98059 did not show apoptosis.CONCLUSION: IGF-IR and PI3K are good candidates for molecular therapy of pancreatic cancer. 展开更多
关键词 insulin-like growth factor-I receptor Phosphatidylinositol 3 kinase Pancreatic neoplasms
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Reactivation of the insulin-like growth factor-Ⅱsignaling pathway in human hepatocellular carcinoma 被引量:40
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作者 Kai Breuhahn Peter Schirmacher 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第11期1690-1698,共9页
Constitutive activation of the insulin-like growth factor (IGF)-signaling axis is frequently observed in human hepatocellular carcinoma(HCC).Especially the over- expression of the fetal growth factor IGF-Ⅱ,IGF-Ⅰ rec... Constitutive activation of the insulin-like growth factor (IGF)-signaling axis is frequently observed in human hepatocellular carcinoma(HCC).Especially the over- expression of the fetal growth factor IGF-Ⅱ,IGF-Ⅰ receptor(IGF-IR),and cytoplasmic downstream effectors such as insulin-receptor substrates(IRS)contribute to proliferation,anti-apoptosis,and invasive behavior. This review focuses on the relevant alterations in this signaling pathway and independent in vivo models that support the central role IGF-Ⅱsignaling during HCC development and progression.Since this pathway has become the center of interest as a target for potential anti-cancer therapy in many types of malignancies,various experimental strategies have been developed,including neutralizing antibodies and selective receptor kinase inhibitors,with respect to the specific and efficient reduction of oncogenic IGF-Ⅱ/IGF-IR-signaling. 展开更多
关键词 Hepatocellular carcinoma insulin-like growth factor-Ⅱ insulin-like growth factor-Ⅰ receptor Insulin receptor substrate House models THERAPY
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Insulin-like growth factor receptor-1 overexpression is associated with poor response of rectal cancers to radiotherapy 被引量:5
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作者 Xiao-Yu Wu Zhen-Feng Wu +7 位作者 Qin-Hong Cao Che Chen Zhi-Wei Chen Zhe Xu Wei-Su Li Fu-Kun Liu Xue-Quan Yao Gang Li 《World Journal of Gastroenterology》 SCIE CAS 2014年第43期16268-16274,共7页
AIM: To explore the potential correlation between insulin-like growth factor receptor-1 (IGF-1R) expression and rectal cancer radiosensitivity.
关键词 insulin-like growth factor-1 receptor Rectal carcinoma Preoperative radiotherapy IMMUNOHISTOCHEMISTRY Reverse transcription-polymerase chain reaction
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Epigenetic regulation of insulin-like growth factor axis in hepatocellular carcinoma 被引量:3
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作者 Hend Mohamed El Tayebi Ahmed Ihab Abdelaziz 《World Journal of Gastroenterology》 SCIE CAS 2016年第9期2668-2677,共10页
The insulin-like growth factor(IGF) signaling path-way is an important pathway in the process of hepa-tocarcinogenesis,and the IGF network is clearly dysregulated in many cancers and developmental abnormalities.In hep... The insulin-like growth factor(IGF) signaling path-way is an important pathway in the process of hepa-tocarcinogenesis,and the IGF network is clearly dysregulated in many cancers and developmental abnormalities.In hepatocellular carcinoma(HCC),only a minority of patients are eligible for curative treatments,such as tumor resection or liver transplant.Unfortunately,there is a high recurrence of HCC after surgical tumor removal.Recent research efforts have focused on targeting IGF axis members in an attempt to find therapeutic options for many health problems.In this review,we shed lights on the regulation of members of the IGF axis,mainly by micro RNAs in HCC.Micro RNAs in HCC attempt to halt the aberrant expression of the IGF network,and a single micro RNA can have multiple downstream targets in one or more signaling pathways.Targeting micro RNAs is a relatively new approach for identifying an efficient radical cure for HCC. 展开更多
关键词 Hepatocellular carcinoma insulin-like growth factors insulin-like growth factor receptors EPIGENETICS MICRORNAS
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Role of Insulin-like Growth Factor II Receptor in Transdifferentiation of Free Silica-induced Primary Rat Lung Fibroblasts 被引量:4
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作者 HAO Chang Fu LI Xiao Fang YAO Wu 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2013年第12期979-985,共7页
Objective To study the role of insulin-like growth factor II receptor in free silica-induced transdifferentiation of primary rat lung fibroblasts Methods Rat lung fibroblasts and rat alveolar macrophages were cultured... Objective To study the role of insulin-like growth factor II receptor in free silica-induced transdifferentiation of primary rat lung fibroblasts Methods Rat lung fibroblasts and rat alveolar macrophages were cultured. A transdifferentiation model of primary rat lung fibroblasts was induced by free silica. Levels of a-SMA protein, IGF-liR protein and mRNA were measured by immunocytochemistry, Western blot and RT-PCR, respectively. Lung fibroblasts were treated with Wortmannin. Results The expression levels of a-SMA concentration and decreased after Wortmann and IGF-IIR increased with the increasing free silica n was used. Conclusion The IGF-IIR plays an important role in free silica-induced transdifferentiation of primary rat lung fibroblasts. 展开更多
关键词 TRANSDIFFERENTIATION Lung fibroblasts insulin-like growth factor II receptor SILICOSIS
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Abnormal expression of insulin-like growth factor-Ⅱ and its dynamic quantitative analysis at different stages of hepatocellular carcinoma development 被引量:16
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《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2008年第4期406-411,共6页
BACKGROUND:Hepatocellular carcinoma(HCC)is characterized by multiple causes,clear multiple stages and a multifocal process of tumor progression related intimately to the overexpression of many cellular factors. The ai... BACKGROUND:Hepatocellular carcinoma(HCC)is characterized by multiple causes,clear multiple stages and a multifocal process of tumor progression related intimately to the overexpression of many cellular factors. The aim of this study was to investigate the dynamic expression of insulin-like growth factor-Ⅱ(IGF-Ⅱ) and its abnormal alteration in the early stages of HCC development. METHODS:Hepatoma models were induced by 2-fluorenylacetamide(2-FAA)in male Sprague-Dawley rats.Morphological changes of rat livers were assessed by pathological examination(HE staining).The levels of IGF-Ⅱexpression in the livers and sera of rats were quantitatively detected by an enzyme-linked immunosorbent assay(ELISA).Simultaneously,the expression and cellular distribution of liver IGF-Ⅱwere analyzed by immunohistochemistry. RESULTS:Histological examination confirmed that rat hepatocytes showed changes from granule-like degeneration to atypical hyperplasia to HCC,and progressively increasing hepatic IGF-Ⅱlevels during HCC development.The levels of hepatic or serum IGF- Ⅱin HCC tissues and sera were significantly higher than those in normals and rats with degeneration.The immunohistochemical evidence indicated the positiveexpression and hepatocyte distribution of IGF-Ⅱin rat hepatoma.A positive relationship of IGF-Ⅱlevels was found between liver tissues and sera of experimental rats (P【0.01). CONCLUSION:Hepatic IGF-Ⅱmay participate in hepatocyte cancer development and detection of IGF-Ⅱ expression during HCC development could be a useful molecular marker for its early diagnosis. 展开更多
关键词 HEPATOCELLULAR carcinoma insulin-like growth factor-Ⅱ IMMUNOHISTOCHEMISTRY DYNAMIC EXPRESSION
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Effect of endogenous insulin-like growth factor and stem cell factor on diabetic colonic dysmotility 被引量:18
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作者 Yun Wang Xin-Yu Xu +5 位作者 Yu-Rong Tang Wei-Wei Yang Yu-Feng Yuan Yue-Ji Ning Yin-Juan Yu Lin Lin 《World Journal of Gastroenterology》 SCIE CAS 2013年第21期3324-3331,共8页
AIM: To investigate whether the reduction of stem cell factor (SCF) is mediated by decreased endogenous insulin-like growth factor (IGF)-1 in diabetic rat colon smooth muscle. METHODS: Sixteen Sprague-Dawley rats were... AIM: To investigate whether the reduction of stem cell factor (SCF) is mediated by decreased endogenous insulin-like growth factor (IGF)-1 in diabetic rat colon smooth muscle. METHODS: Sixteen Sprague-Dawley rats were randomly divided into two groups: control group and streptozotocin-induced diabetic group. After 8 wk of streptozotocin administration, colonic motility function and contractility of circular muscle strips were measured. The expression of endogenous IGF-1 and SCF was tested in colonic tissues. Colonic smooth muscle cells were cultured from normal adult rats. IGF-1 siRNA transfection was used to investigate whether SCF expression was affected by endogenous IGF-1 expression in smooth muscle cells, and IGF-1 induced SCF expression effects were studied. The effect of high glucose on the expression of endogenous IGF-1 and SCF was also investigated. RESULTS: Diabetic rats showed prolonged colonic transit time (252 ± 16 min vs 168 ± 9 min, P < 0.01) and weakness of circular muscle contraction (0.81 ± 0.09 g vs 2.48 ± 0.23 g, P < 0.01) compared with the control group. Endogenous IGF-1 and SCF protein expression was significantly reduced in the diabetic colonic muscle tissues. IGF-1 and SCF mRNA expression also showed a paralleled reduction in diabetic rats. In the IGF-1 siRNA transfected smooth muscle cells, SCF mRNA and protein expression was significantly decreased. IGF-1 could induce SCF expression in a concentration and time-dependent manner, mainly through the extracellular-signal-regulated kinase 1/2 signal pathway. High glucose inhibited endogenous IGF-1 and SCF expression and the addition of IGF-1 to the medium reversed the SCF expression. CONCLUSION: Myopathy may resolve in colonic motility dysfunction in diabetic rats. Deficiency of endogenous IGF-1 in colonic smooth muscle cells leads to reduction of SCF expression. 展开更多
关键词 Diabetes GASTROINTESTINAL MOTILITY function insulin-like growth factor-1 Stem CELL factor Smooth muscle CELL
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Overexpression of insulin-like growth factor-Ⅰ receptor as a pertinent biomarker for hepatocytes malignant transformation 被引量:18
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作者 Xiao-Di Yan Min Yao +7 位作者 Li Wang Hai-Jian Zhang Mei-Juan Yan Xing Gu Yun Shi Jie Chen Zhi-Zhen Dong Deng-Fu Yao 《World Journal of Gastroenterology》 SCIE CAS 2013年第36期6084-6092,共9页
AIM: To investigate the dynamic features of insulin-like growth factor-I receptor (IGF-IR) expression in rat hepatocarcinogenesis, and the relationship between IGF-IR and hepatocytes malignant transformation at mRNA o... AIM: To investigate the dynamic features of insulin-like growth factor-I receptor (IGF-IR) expression in rat hepatocarcinogenesis, and the relationship between IGF-IR and hepatocytes malignant transformation at mRNA or protein level.METHODS: Hepatoma models were made by inducing with 2-fluorenylacetamide (2-FAA) on male Sprague-Dawley rats. Morphological changes of hepatocytes were observed by pathological Hematoxylin and eosin staining, the dynamic expressions of liver and serum IGF-IR were quantitatively analyzed by an enzyme-linked immunosorbent assay. The distribution of hepatic IGF-IR was located by immunohistochemistry. The fragments of IGF-IR gene were amplified by reverse transcription-polymerase chain reaction, and confirmed by sequencing.RESULTS: Rat hepatocytes after induced by 2-FAA were changed dynamically from granule-like degeneration, precancerous to hepatoma formation with the progressing increasing of hepatic mRNA or IGF-IR expression. The incidences of liver IGF-IR, IGF-IR mRNA, specific IGF-IR concentration (ng/mg wet liver), and serum IGF-IR level (ng/mL) were 0.0%, 0.0%, 0.63 ± 0.17, and 1.33 ± 0.47 in the control; 50.0%, 61.1%, 0.65 ± 0.2, and 1.51 ± 0.46 in the degeneration; 88.9%, 100%, 0.66 ± 0.14, and 1.92 ± 0.29 in the precancerosis; and 100%, 100%, 0.96 ± 0.09, and 2.43 ± 0.57 in the cancerous group, respectively. IGF-IR expression in the cancerous group was significantly higher (P < 0.01) than that in any of other groups at mRNA or protein level. The closely positive IGF-IR relationship was found between livers and sera (r = 0.91, t = 14.222, P < 0.01), respectively.CONCLUSION: IGF-IR expression may participate in rat hepatocarcinogenesis and its abnormality should be an early marker for hepatocytes malignant transformation. 展开更多
关键词 HEPATOMA insulin-like growth factor-I receptor IMMUNOHISTOCHEMISTRY Gene amplification SEQUENCING Rat hepatoma model
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Mitochondrial protection by low doses of insulin-like growth factor-Ⅰin experimental cirrhosis 被引量:11
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作者 Raquel Pérez María García-Fernández +5 位作者 Matías Díaz-Sánchez Juan E Puche Gloria Delgado Marian Conchillo Jordi Muntané Inma Castilla-Cortázar 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第17期2731-2739,共9页
AIM: To characterize the mitochondrial dysfunction in experimental cirrhosis and to study whether insulin-like growth factor-Ⅰ (IGF-Ⅰ ) therapy (4 wk) is able to induce beneficial effects on damaged mitochondri... AIM: To characterize the mitochondrial dysfunction in experimental cirrhosis and to study whether insulin-like growth factor-Ⅰ (IGF-Ⅰ ) therapy (4 wk) is able to induce beneficial effects on damaged mitochondria leading to cellular protection. METHODS: Wistar rats were divided into three groups: Control group, untreated cirrhotic rats and cirrhotic rats treated with IGF-Ⅰ treatment (2 μg/1O0 g bw/d). Mitochondrial function was analyzed by flow cytometry in isolated hepatic mitochondria, caspase 3 activation was assessed by Western blot and apoptosis by TUNEL in the three expedmental groups. RESULTS: Untreated cirrhotic rats showed a mitochondrial dysfunction characterized by a significant reduction of mitochondrial membrane potential (in status 4 and 3); an increase of intramitochondrial reactive oxigen species (ROS) generation and a significant reduction of ATPase activity. IGF-Ⅰ therapy normalized mitochondrial function by increasing the membrane potential and ATPase activity and reducing the intramitochondrial free radical production. Activity of the electron transport complexes Ⅰ and Ⅲ was increased in both cirrhotic groups. In addition, untreated cirrhotic rats showed an increase of caspase 3 activation and apoptosis. IGF- Ⅰ therapy reduced the expression of the active peptide of caspase 3 and resulted in reduced apoptosis. CONCLUSION: These results show that IGF- Ⅰ exerts a mitochondrial protection in experimental cirrhosis leading to reduced apoptosis and increased ATP production. 展开更多
关键词 insulin-like growth factor- CIRRHOSIS Mitochondrial protection CASPASES APOPTOSIS Oxidativedamage
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Effects of Insulin-like Growth Factor 1 Receptor and Its Inhibitor AG1024 on the Progress of Lung Cancer 被引量:3
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作者 魏艳红 唐和孝 +9 位作者 廖永德 付圣灵 徐利强 陈广 张超 具晟 刘昭国 游良坤 喻莉 周晟 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2015年第6期834-841,共8页
Summary: The type 1 insulin-like growth factor receptor (IGF-1R) and its downstream signaling com- ponents have been increasingly recognized to drive the development of malignancies, including non-small cell lung c... Summary: The type 1 insulin-like growth factor receptor (IGF-1R) and its downstream signaling com- ponents have been increasingly recognized to drive the development of malignancies, including non-small cell lung cancer (NSCLC). This study aimed to investigate the effects of IGF-1R and its in- hibitor, AG1024, on the progression of lung cancer. Tissue microarray and immunohistochemistry were employed to detect the expressions of IGF-1 and IGF-1R in NSCLC tissues (n=198). Western blotting was used to determine the expressions oflGF-1 and phosphorylated IGF-1R (p-IGF-1R) in A549 human lung carcinoma cells, and MTT assay to measure cell proliferation. Additionally, the expressions of IGF-1, p-IGF-1R and IGF-1R in a mouse model of lung cancer were detected by Western blotting and real-time fluorescence quantitative polymerase chain reaction (FQ-PCR), respectively. The results showed that IGF-1 and IGF-1R were overexpressed in NSCLC tissues. The expression levels of IGF-1 and p-IGF-1R were significantly increased in A549 cells treated with IGF-1 as compared to those treated with IGF-1 +AG 1024 or untreated cells. In the presence of IGF-1, the proliferation of A549 cells was significantly increased. The progression of lung cancer in mice treated with IGF-1 was significantly increased as compared to the group treated with IGF-l+AG1024 or the control group, with the same trend mirrored in IGF-1/p-IGF-1R/IGF-1R at the protein and/or mRNA levels. It was concluded that IGF- 1 and IGF inhibitor AG 1024 promotes lung cancer progression. 展开更多
关键词 lung cancer mouse lung adenocarcinoma model insulin-like growth factor-1 receptor AG 1024
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Insulin-like growth factor-1, IGF binding protein-3, and the risk of esophageal cancer in a nested case-control study 被引量:6
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作者 Yasushi Adachi Masanori Nojima +7 位作者 Mitsuru Mori Kentaro Yamashita Hiro-o Yamano Hiroshi Nakase Takao Endo Kenji Wakai Kiyomi Sakata Akiko Tamakoshi 《World Journal of Gastroenterology》 SCIE CAS 2017年第19期3488-3495,共8页
To assess the relationship between serum levels of insulin-like growth factor-1 (IGF1)/IGF-binding protein-3 (IGFBP3) and the risk of esophageal carcinoma.METHODSWe assessed the relationship between the serum levels o... To assess the relationship between serum levels of insulin-like growth factor-1 (IGF1)/IGF-binding protein-3 (IGFBP3) and the risk of esophageal carcinoma.METHODSWe assessed the relationship between the serum levels of these molecules and the risk of esophageal cancer in a prospective, nested case-control study of participants from the Japan Collaborative Cohort Study. A baseline survey was conducted from 1988 to 1990. Of the 110585 enrolled participants, 35% donated blood samples. Those who had been diagnosed with esophageal cancer were considered cases for nested case-control studies. A conditional logistic model was used to estimate odds ratios for the incidence of esophageal cancer associated with serum IGF1 and IGFBP3 levels.RESULTSThirty-one cases and 86 controls were eligible for the present assessment. The molar ratio of IGF1/IGFBP3, which represents the free and active form of IGF1, was not correlated with the risk of esophageal carcinoma. A higher molar difference between IGFBP3 and IGF1, which estimates the free form of IGFBP3, was associated with a decreased risk of esophageal carcinoma (P = 0.0146), and people in the highest tertile had the lowest risk (OR = 0.107, 95%CI: 0.017-0.669). After adjustment for body mass index, tobacco use, and alcohol intake, the molar difference of IGFBP3-IGF1 was inversely correlated with the risk of esophageal carcinoma (P = 0.0150).CONCLUSIONThe free form of IGFBP3, which is estimated by this molar difference, may be inversely associated with esophageal cancer incidence. 展开更多
关键词 Esophageal cancer insulin-like growth factor insulin-like growth factor binding protein Nested case-control study Odds ratio
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Effects of Bifidobacterium infantis on cytokine-induced neutrophil chemoattractant and insulin-like growth factor-1 in the ileum of rats with endotoxin injury 被引量:7
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作者 Wei Wang Mei Sun +2 位作者 Yu-Ling Zheng Liu-Yu Sun Shu-Qiang Qu 《World Journal of Gastroenterology》 SCIE CAS 2019年第23期2924-2934,共11页
BACKGROUND The digestive tract is the maximal immunizing tissue in the body, and mucosal integrity and functional status of the gut is very important to maintain a healthy organism. Severe infection is one of the most... BACKGROUND The digestive tract is the maximal immunizing tissue in the body, and mucosal integrity and functional status of the gut is very important to maintain a healthy organism. Severe infection is one of the most common causes of gastrointestinal dysfunction, and the pathogenesis is closely related to endotoxemia and intestinal barrier injury. Bifidobacterium is one of the main probiotics in the human body that is involved in digestion, absorption, metabolism, nutrition, and immunity.Bifidobacterium plays an important role in maintaining the intestinal mucosal barrier integrity. This study investigated the protective mechanism of Bifidobacterium during ileal injury in rats.AIM To investigate the effects of Bifidobacterium on cytokine-induced neutrophil chemoattractant(CINC) and insulin-like growth factor 1(IGF-1) in the ileum of rats with endotoxin injury.METHODS Preweaning rats were randomly divided into three groups: Control(group C),model(group E) and treatment(group T). Group E was intraperitoneally injected with lipopolysaccharide(LPS) to create an animal model of intestinal injury.Group T was intragastrically administered Bifidobacterium suspension 7 d before LPS. Group C was intraperitoneally injected with normal saline. The rats were killed at 2, 6 or 12 h after LPS or physiological saline injection to collect ilealtissue samples. The expression of ileal CINC mRNA was evaluated by reverse transcription-polymerase chain reaction(RT-PCR), and expression of ileal IGF-1 protein and mRNA was detected by immunohistochemistry and RT-PCR,respectively.RESULTS The ileum of rats in Group C did not express CINC mRNA, ileums from Group E expressed high levels, which was then significantly decreased in Group T(F =23.947, P < 0.05). There was no significant difference in CINC mRNA expression at different times(F = 0.665, P > 0.05). There was a high level of IGF-1 brown granules in ileal crypts and epithelial cells in Group C, sparse staining in Group E, and dark, dense brown staining in Group T. There was a significant difference between Groups C and E and Groups E and T(P < 0.05). There was no significant difference in IGF-1 protein expression at different times(F = 1.269, P > 0.05). IGF-1 mRNA expression was significantly different among the three groups(P < 0.05),though not at different times(F = 0.086, P > 0.05).CONCLUSION Expression of CINC mRNA increased in the ileum of preweaning rats with endotoxin injury, and exogenous administration of Bifidobacterium reduced CINC m RNA expression. IGF-1 protein and mRNA expression decreased in the ileum of preweaning rats with endotoxin injury, and exogenous administration of Bifidobacterium prevented the decrease in IGF-1 expression. Bifidobacterium may increase IGF-1 expression and enhance intestinal immune barrier function in rats with endotoxin injury. 展开更多
关键词 BIFIDOBACTERIUM ILEUM Cytokine-induced neutrophil CHEMOATTRACTANT insulin-like growth factor-1 RATS
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Effect of sericin on diabetic hippocampal growth hormone/insulin-like growth factor 1 axis 被引量:2
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作者 Zhihong Chen Songhe Yang +2 位作者 Yaqiang He Chengjun Song Yongping Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第19期1756-1764,共9页
Previous studies have shown that sericin extracted from silk cocoon significantly reduces blood glucose levels and protects the nervous system against diabetes mellitus. In this study, a rat type 2 diabetes mellitus m... Previous studies have shown that sericin extracted from silk cocoon significantly reduces blood glucose levels and protects the nervous system against diabetes mellitus. In this study, a rat type 2 diabetes mellitus model was established by intraperitoneal injection of 25 mg/kg streptozotocin for 3 successive days, following which the rats were treated with sericin for 35 days. After treatment, the blood glucose levels of the diabetic rats decreased significantly, the growth hormone level in serum and its expression in the hippocampus decreased significantly, while the insulin-like growth factor-1 level in serum and insulin-like growth factor-1 and growth hormone receptor expression in the hippocampus increased significantly. The experimental findings indicate that sericin improves disorders of the growth hormone/insulin-like growth factor 1 axis to alleviate hippocampal damage in diabetic rats. 展开更多
关键词 neural regeneration traditional Chinese medicine SERICIN type 2 diabetes mellitus hippocampus growth hormone insulin-like growth factor 1 growth hormone receptor growth hormone/insulin-likegrowth factor 1 axis STREPTOZOTOCIN blood glucose western blot assay reverse transcription-PCR grants-supported paper NEUROREGENERATION
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