BACKGROUND MicroRNA 34c(miR-34c)has been reported to be associated with malignant types of cancer,however,it remains unknown whether miR-34c is involved in chemoresistance in gastric cancer(GC).AIM To investigate the ...BACKGROUND MicroRNA 34c(miR-34c)has been reported to be associated with malignant types of cancer,however,it remains unknown whether miR-34c is involved in chemoresistance in gastric cancer(GC).AIM To investigate the effect of miR-34c and its upstream transcription factor E2F1 on paclitaxel combined with cisplatin resistance in GC cells.METHODS Paired GC tissues and adjacent normal tissues were randomly sampled from 74 GC patients.miR-34c and E2F1 were detected by real-time quantitative PCR(qPCR)and Western blot.In addition,the drug resistance of GC cells to paclitaxel and cisplatin was induced by concentration gradient increasing methods,and changes in miR-34c and E2F1 during this process were measured.Furthermore,E2F1 and miR-34c overexpression or underexpression vectors were constructed and transfected into drug-resistant GC cells.MTT was employed to test the sensitivity of cells to paclitaxel combined with cisplatin,qPCR was adopted to detect the expression of miR-34c,Western blot was applied to detect the expression levels of E2F1,drug resistance-related proteins and apoptosis-related proteins,and flow cytometry was used for the determination of cell apoptosis and cell cycle status.RESULTS E2F1 was overexpressed while miR-34c was underexpressed in GC.After inducing GC cells to be resistant to paclitaxel and cisplatin,E2F1 expression increased while miR-34c expression decreased.Both silencing E2F1 and overexpressing miR-34c could increase the sensitivity of drug-resistant GC cells to paclitaxel combined with cisplatin,promote cell apoptosis and inhibit cell proliferation.Among which,silencing E2F1 could reduce the expression of drug resistance-related proteins and apoptosis-related proteins,while over-expression of miR-34c could upregulate the expression of apoptosis-related proteins without affecting the expression of MDR-1,MRP and other drug resistance-related proteins.Rescue experiments demonstrated that inhibiting miR-34c could significantly weaken the sensitization of drug resistant cells,and Si E2F1 to paclitaxel combined with cisplatin.CONCLUSION E2F1 inhibits miR-34c to promote the proliferation of GC cells and enhance the resistance to paclitaxel combined with cisplatin,and silencing E2F1 is conducive to improving the efficacy of paclitaxel combined with cisplatin in GC cells.展开更多
AIM: To investigate the association between endogenous gene expression and growth regulation including proliferation and apoptosis induced by transforming growth factor-pi (TGF-βl) in human gastric cancer (GC) cells....AIM: To investigate the association between endogenous gene expression and growth regulation including proliferation and apoptosis induced by transforming growth factor-pi (TGF-βl) in human gastric cancer (GC) cells. METHODS: Reverse transcription polymerase chain reaction (RT-PCR) was performed to detect the main components of the TGF-β1/Smads signal pathway in human poorly differentiated GC cell line BGC-823. Localization of Smad proteins was also determined using immunofluorescence. Then, the BGC-823 cells were cultured in the presence or absence of TGF-β1 (10 ng/mL) for 24 and 48 h, and the effects of TGF-β1 on proliferation and apoptosis were measured by cell growth curve and flow cytometry (FCM) analysis. The ultrastructural features of BGC-823 cells with or without TGF-β1 treatment were observed under transmission electron microscope. The apoptotic cells were visualized by means of the terminal deoxynucleotidyl transferase (TdT)-mediated dTUP in situ nick end-labeling (TUNEL) method. Meanwhile, the expression levels of endogenous p15, p21 and Smad7 mRNA and the corresponding proteins in the cells were detected at 1, 2 and 3 h after culture in the presence or absence of TGF-β1 (10 ng/mL) by semi-quantitative RT-PCR and Western blot, respectively. RESULTS: The TGF-β1/Smad signaling was found to be intact and functional in BGC-823 cells. The growth curve revealed the most evident inhibition of cell proliferation by TGF-β1 at 48 h, and FCM assay showed G1 arrest accompanied with apoptosis induced by TGF-β1. The typical morphological changes of apoptosis were observed in cells exposed to TGF-β1. The apoptosis index (AI) in TGF-β1-treated cells was significantly higher than that in the untreated controls (10.7±1.3% vs 0.32±0.06%, P＜0.01). The levels of p15, p21 and Smad7mRNA and corresponding proteins in cells were significantly up-regulated at 1 h, but gradually returned to basal levels at 3 h following TGF-βl (10 ng/mL) treatment. CONCLUSION: TGF-β1 affects both proliferation and apoptosis of GC cells through the regulation of p15 and p21, and induces transient expression of Smad 7 as a negative feedback modulation of TGF-β1 signal. Our results suggest a novel functional role of p21 as an accelerant of TGF-β1-mediated apoptosis in GC cells.展开更多
AIM: To clarify the role of high in normal-1 (HIN-1) gene promoter methylation during gastric cancer development. METHODS: Gastric cancer cell lines and tissue specimens were analyzed for expression of HIN-1 mRNA and ...AIM: To clarify the role of high in normal-1 (HIN-1) gene promoter methylation during gastric cancer development. METHODS: Gastric cancer cell lines and tissue specimens were analyzed for expression of HIN-1 mRNA and protein using the semi-quantitative reverse transcription polymerase chain reaction and immunohistochemistry. The methylation of the HIN-1 gene promoter was detected in gastric carcinoma cells and tissues using methylation-specific polymerase chain reaction. The 3-(4,5-dimethylthiazol-2yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium cell viability assay and flow cytometry were used to assess the changes in behaviors of gastric cancer cells with or without 5-aza-2’-deoxycytidine treatment. RESULTS: HIN-1 was not expressed in 4 of 5 gastric cancer cell lines. The demethylation reagent 5-aza-2’-deoxycytidine was able to induce or upregulate HIN-1 expression in gastric cancer cell lines, which is associated with reduction of tumor cell viability. Furthermore, methylation of the HIN-1 gene promoter was shown in 57.8% (26/45) of the primary gastric cancer and 42.1% (17/38) of adjacent tissue samples, but was not shown in normal gastric mucosa (0/10). From the clinicopathological data of the patients, methylation of the HIN-1 gene promoter was found to be associated with tumor differentiation (P = 0.000). CONCLUSION: High methylation of HIN-1 gene promoter results in silence of HIN-1 expression in gastric cancer. 5-aza-2’-deoxycytidine reverses HIN-1 methylation and reduces viability of gastric cancer cells.展开更多
BACKGROUND Phosphatidylinositol-3,4,5-trisphosphate dependent Rac exchange factor 1(PREX1)was reported to be overexpressed in some cancers and involved in cancer development,but its expression and significance in gast...BACKGROUND Phosphatidylinositol-3,4,5-trisphosphate dependent Rac exchange factor 1(PREX1)was reported to be overexpressed in some cancers and involved in cancer development,but its expression and significance in gastric cancer remain unclear.AIM To evaluate the expression of PREX1 in gastric cancer and its significance in the development of gastric cancer,especially to evaluate the potential mechanism of PREX1 in gastric cancer.METHODS Bioinformatic analysis was performed in order to examine the expression of PREX1 in gastric cancer.The relationship between the survival rate of gastric cancer patients and PREX1 expression was assessed by Kaplan Meier portal.The Gene Set Enrichment Analysis and the correlation between PREX1 and transforming growth factor(TGF)β1 pathway-related mediators were evaluated by cBioPortal for Cancer Genomics.Western blotting and reverse transcriptase polymerase chain reaction assay were used to test the role of TGFβ1 on the expression of PREX1.Western blotting and dual-luciferase reporter system was used to evaluate the effect of PREX1 on the activation of TGFβ1 pathway.Wound healing and Transwell assay were used to assess the effect of PREX1 on the metastasis activity of gastric cancer cells.RESULTS PREX1 was overexpressed in the gastric tumors,and the expression levels were positively associated with the development of gastric cancer.Also,the high expression of PREX1 revealed poor prognosis,especially for those advanced and specific intestinal gastric cancer patients.PREX1 was closely involved in the positive regulation of cell adhesion and positively correlated with TGFβ1-related mediators.Furthermore,TGFβ1 could induce the expression of PREX1 at both the protein and mRNA level.Also,PREX1 could activate the TGFβ1 pathway.The induced PREX1 could increase the migration and invasion activity of gastric cancer cells.CONCLUSION PREX1 is overexpressed in gastric cancer,and the high level of PREX1 predicts poor prognosis.PREX1 is closely associated with TGFβsignaling and promotes the metastasis of gastric cancer cells.展开更多
Objective： MicroRNAs （miRNAs） are important regulators that play a key role in tumorigenesis and rumor progression. Transforming growth factor-β1 （TGF-β1） is involved in invasion and metastasis in many tumors. ...Objective： MicroRNAs （miRNAs） are important regulators that play a key role in tumorigenesis and rumor progression. Transforming growth factor-β1 （TGF-β1） is involved in invasion and metastasis in many tumors. In this study, we investigated the microRNAs （miRNA） profiles altered by TGF-β1 in gastric cancer （GC） cells. Methods： We detected the expression profiles of miRNA by miRNA microarray and quantitative real- time polymerase chain reaction. Migration and invasion, wound-healing assay, prediction of miRNA targets, Western blot and qRT-PCR analysis were carried out to determine the role of one selected miRNA, namely miR-193b, in affecting the biological behaviors of GC BGC823 cells. Results： Among 847 human miRNAs in the microarray, three miRNAs （miR-27a, miR-29b-1 and miR-194） were up-regulated and three （miR-574-3p, miR-193b and miR-130b） were down-regulated in BGC823 cells treated with TGF-β1 compared with control, miR-193b suppressed the invasion and metastasis of GC cells in vivo and in vitro, and down-regulated urokinase-type plasminogen activator （uPA） protein in GC cells. Conclusions： TGF-β1 altered miRNA expression profile in BGC823 cells. Among the altered miRNAs, TGF-β1 induced the down-regulation of miR-193b, which inhibited cell invasion and metastasis in vivo and in vitro, and down-regulated uPA protein in GC cells.展开更多
目的探讨胃癌组织中核转录因子-κB(nuclear factor kappa B,NF-κB)、程序性细胞死亡蛋白-1(programmed cell death protein-1,PD-1)、程序性细胞死亡蛋白配体-1(programmed cell death protein ligand 1,PD-L1)的表达及其临床意义。...目的探讨胃癌组织中核转录因子-κB(nuclear factor kappa B,NF-κB)、程序性细胞死亡蛋白-1(programmed cell death protein-1,PD-1)、程序性细胞死亡蛋白配体-1(programmed cell death protein ligand 1,PD-L1)的表达及其临床意义。方法选择2021年1月至2023年12月于南阳市第一人民医院治疗的62例胃癌患者手术切除后组织标本及癌旁正常组织标本分别作为胃癌组及癌旁组。62例患者中,男39例,女23例,年龄(61.86±2.31)岁,肿瘤长径(4.92±0.53)cm。采用免疫组织化学染色法检测NF-κB、PD-1、PD-L1表达情况。比较两组NF-κB、PD-1、PD-L1表达阳性率,分析其与胃癌临床病理特征的关系。采用χ^(2)检验。结果胃癌组NF-κB、PD-1、PD-L1表达阳性率高于癌旁组[83.87%(52/62)比33.87%(21/62)、75.81%(47/62)比30.65%(19/62)、80.65%(50/62)比40.32%(25/62)],差异均有统计学意义(χ^(2)=32.008、25.396、21.088,均P<0.05);肌层及浆膜层浸润、有淋巴结转移及Ⅲ+Ⅳ期患者NF-κB表达阳性率高于黏膜及黏膜下层浸润、无淋巴结转移及Ⅰ+Ⅱ期患者[92.68%(38/41)比66.67%(14/21)、94.74(36/38)比66.67%(16/24)、92.31%(36/39)比69.57%(16/23)],差异均有统计学意义(χ^(2)=5.158、6.619、3.978,均P<0.05);肌层及浆膜层浸润、有淋巴结转移及Ⅲ+Ⅳ期患者PD-1表达阳性率高于黏膜及黏膜下层浸润、无淋巴结转移及Ⅰ+Ⅱ期患者[85.37%(35/41)比57.14%(14/21)、89.47%(34/38)比54.17%(13/24)、89.74%(35/39)比52.17%(12/23)],差异均有统计学意义(χ^(2)=6.031、9.998、11.135,均P<0.05);低分化、肌层及浆膜层浸润、有淋巴结转移及Ⅲ+Ⅳ期患者PD-L1表达阳性率高于高中分化、黏膜及黏膜下层浸润、无淋巴结转移及Ⅰ+Ⅱ期患者[96.00%(24/25)比70.27%(26/37)、90.24%(37/41)比61.90%(13/21)、92.11%(35/38)比62.50%(15/24)、94.87%(37/39)比56.52%(13/23)],差异均有统计学意义(χ^(2)=4.787、5.445、6.472、11.286,均P<0.05)。结论胃癌组织中NF-κB、PD-1、PD-L1表达阳性率升高,且NF-κB、PD-1表达与胃癌浸润深度、淋巴结转移及TNM分期有关,PD-L1表达与胃癌分化程度、浸润深度、淋巴结转移及TNM分期有关。展开更多
AIM: To investigate the expression of gastrokine 1 (GKN1) in normal gastric mucosa, precancerous lesions and gastric cancer tissues, and to analyse its correlations with tumour site and pathological pattern.
Objective:To study the expression and significance of TNF-transcription factor M1(FoxM1)in bladder cancer and cystitis glandularis(CG).Methods:A total of 30 patients with bladder cancer admitted to our hospital and re...Objective:To study the expression and significance of TNF-transcription factor M1(FoxM1)in bladder cancer and cystitis glandularis(CG).Methods:A total of 30 patients with bladder cancer admitted to our hospital and received surgical treatment from February 2017 to February 2019 were included for the study.During surgery,bladder cancer tissues and normal bladder tissues(tissues more than 5cm away from the cancer tissue center)were collected.Meanwhile,we retained 30 CG tissues from 30 CG patients who received surgical treatment in our hospital at the same time.Bladder cancer cell lines RT4 and BIU87 were cultured and treated with TNF-αat different concentrations(0nM,1nM,5nM,10nM).The expressions of TNF-αand FoxM1 in different bladder tissues were analyzed,and the effects of different concentrations of TNF-αon the expressions of FoxM1 in bladder cancer cell lines and cyclin B1 and cyclin D1 in bladder cancer cell lines were analyzed.Results:The expression levels of TNF-αand FoxM1 in normal bladder,CG and bladder cancer tissues were gradually increased,and univariate analysis of variance showed that the differences between groups were statistically significant(all P<0.05).FoxM1 expression in bladder cancer cell lines treated with TNF-αat concentrations of 0nM,1nM,5nM and 10nM showed a gradual increase trend,and one-way anova showed that the difference between the groups was statistically significant(all P<0.05).After the treatment of bladder cancer cell lines with TNF-αat concentrations of 0nM,1nM,5nM and 10nM,the expression of cyclin B1 and cyclin D1 showed a gradually increasing trend,and one-way anova showed that the difference between groups was statistically significant(all P<0.05).Conclusion:TNF-αmay play a crucial role in the occurrence and development of CG by regulating the expression of transcription factor FoxM1,and then affecting the expression of cyclin B1 and cyclin D1,which is worthy of clinical attention.展开更多
文摘BACKGROUND MicroRNA 34c(miR-34c)has been reported to be associated with malignant types of cancer,however,it remains unknown whether miR-34c is involved in chemoresistance in gastric cancer(GC).AIM To investigate the effect of miR-34c and its upstream transcription factor E2F1 on paclitaxel combined with cisplatin resistance in GC cells.METHODS Paired GC tissues and adjacent normal tissues were randomly sampled from 74 GC patients.miR-34c and E2F1 were detected by real-time quantitative PCR(qPCR)and Western blot.In addition,the drug resistance of GC cells to paclitaxel and cisplatin was induced by concentration gradient increasing methods,and changes in miR-34c and E2F1 during this process were measured.Furthermore,E2F1 and miR-34c overexpression or underexpression vectors were constructed and transfected into drug-resistant GC cells.MTT was employed to test the sensitivity of cells to paclitaxel combined with cisplatin,qPCR was adopted to detect the expression of miR-34c,Western blot was applied to detect the expression levels of E2F1,drug resistance-related proteins and apoptosis-related proteins,and flow cytometry was used for the determination of cell apoptosis and cell cycle status.RESULTS E2F1 was overexpressed while miR-34c was underexpressed in GC.After inducing GC cells to be resistant to paclitaxel and cisplatin,E2F1 expression increased while miR-34c expression decreased.Both silencing E2F1 and overexpressing miR-34c could increase the sensitivity of drug-resistant GC cells to paclitaxel combined with cisplatin,promote cell apoptosis and inhibit cell proliferation.Among which,silencing E2F1 could reduce the expression of drug resistance-related proteins and apoptosis-related proteins,while over-expression of miR-34c could upregulate the expression of apoptosis-related proteins without affecting the expression of MDR-1,MRP and other drug resistance-related proteins.Rescue experiments demonstrated that inhibiting miR-34c could significantly weaken the sensitization of drug resistant cells,and Si E2F1 to paclitaxel combined with cisplatin.CONCLUSION E2F1 inhibits miR-34c to promote the proliferation of GC cells and enhance the resistance to paclitaxel combined with cisplatin,and silencing E2F1 is conducive to improving the efficacy of paclitaxel combined with cisplatin in GC cells.
基金Supported by the Teaching and Research Award Program for Outstanding Young Teachers in Higher Education Institutions by Ministry of Education and the National Natural Science Foundation of China,No.30370783and the Key Project ofScience and Technology from Heilongjiang Province,No.GB03C601-1
文摘AIM: To investigate the association between endogenous gene expression and growth regulation including proliferation and apoptosis induced by transforming growth factor-pi (TGF-βl) in human gastric cancer (GC) cells. METHODS: Reverse transcription polymerase chain reaction (RT-PCR) was performed to detect the main components of the TGF-β1/Smads signal pathway in human poorly differentiated GC cell line BGC-823. Localization of Smad proteins was also determined using immunofluorescence. Then, the BGC-823 cells were cultured in the presence or absence of TGF-β1 (10 ng/mL) for 24 and 48 h, and the effects of TGF-β1 on proliferation and apoptosis were measured by cell growth curve and flow cytometry (FCM) analysis. The ultrastructural features of BGC-823 cells with or without TGF-β1 treatment were observed under transmission electron microscope. The apoptotic cells were visualized by means of the terminal deoxynucleotidyl transferase (TdT)-mediated dTUP in situ nick end-labeling (TUNEL) method. Meanwhile, the expression levels of endogenous p15, p21 and Smad7 mRNA and the corresponding proteins in the cells were detected at 1, 2 and 3 h after culture in the presence or absence of TGF-β1 (10 ng/mL) by semi-quantitative RT-PCR and Western blot, respectively. RESULTS: The TGF-β1/Smad signaling was found to be intact and functional in BGC-823 cells. The growth curve revealed the most evident inhibition of cell proliferation by TGF-β1 at 48 h, and FCM assay showed G1 arrest accompanied with apoptosis induced by TGF-β1. The typical morphological changes of apoptosis were observed in cells exposed to TGF-β1. The apoptosis index (AI) in TGF-β1-treated cells was significantly higher than that in the untreated controls (10.7±1.3% vs 0.32±0.06%, P＜0.01). The levels of p15, p21 and Smad7mRNA and corresponding proteins in cells were significantly up-regulated at 1 h, but gradually returned to basal levels at 3 h following TGF-βl (10 ng/mL) treatment. CONCLUSION: TGF-β1 affects both proliferation and apoptosis of GC cells through the regulation of p15 and p21, and induces transient expression of Smad 7 as a negative feedback modulation of TGF-β1 signal. Our results suggest a novel functional role of p21 as an accelerant of TGF-β1-mediated apoptosis in GC cells.
基金Supported by National Basic Research Program (973 Program No. 2010CB912802)the Postdoctoral Fund of China, No. 20080441314
文摘AIM: To clarify the role of high in normal-1 (HIN-1) gene promoter methylation during gastric cancer development. METHODS: Gastric cancer cell lines and tissue specimens were analyzed for expression of HIN-1 mRNA and protein using the semi-quantitative reverse transcription polymerase chain reaction and immunohistochemistry. The methylation of the HIN-1 gene promoter was detected in gastric carcinoma cells and tissues using methylation-specific polymerase chain reaction. The 3-(4,5-dimethylthiazol-2yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium cell viability assay and flow cytometry were used to assess the changes in behaviors of gastric cancer cells with or without 5-aza-2’-deoxycytidine treatment. RESULTS: HIN-1 was not expressed in 4 of 5 gastric cancer cell lines. The demethylation reagent 5-aza-2’-deoxycytidine was able to induce or upregulate HIN-1 expression in gastric cancer cell lines, which is associated with reduction of tumor cell viability. Furthermore, methylation of the HIN-1 gene promoter was shown in 57.8% (26/45) of the primary gastric cancer and 42.1% (17/38) of adjacent tissue samples, but was not shown in normal gastric mucosa (0/10). From the clinicopathological data of the patients, methylation of the HIN-1 gene promoter was found to be associated with tumor differentiation (P = 0.000). CONCLUSION: High methylation of HIN-1 gene promoter results in silence of HIN-1 expression in gastric cancer. 5-aza-2’-deoxycytidine reverses HIN-1 methylation and reduces viability of gastric cancer cells.
文摘BACKGROUND Phosphatidylinositol-3,4,5-trisphosphate dependent Rac exchange factor 1(PREX1)was reported to be overexpressed in some cancers and involved in cancer development,but its expression and significance in gastric cancer remain unclear.AIM To evaluate the expression of PREX1 in gastric cancer and its significance in the development of gastric cancer,especially to evaluate the potential mechanism of PREX1 in gastric cancer.METHODS Bioinformatic analysis was performed in order to examine the expression of PREX1 in gastric cancer.The relationship between the survival rate of gastric cancer patients and PREX1 expression was assessed by Kaplan Meier portal.The Gene Set Enrichment Analysis and the correlation between PREX1 and transforming growth factor(TGF)β1 pathway-related mediators were evaluated by cBioPortal for Cancer Genomics.Western blotting and reverse transcriptase polymerase chain reaction assay were used to test the role of TGFβ1 on the expression of PREX1.Western blotting and dual-luciferase reporter system was used to evaluate the effect of PREX1 on the activation of TGFβ1 pathway.Wound healing and Transwell assay were used to assess the effect of PREX1 on the metastasis activity of gastric cancer cells.RESULTS PREX1 was overexpressed in the gastric tumors,and the expression levels were positively associated with the development of gastric cancer.Also,the high expression of PREX1 revealed poor prognosis,especially for those advanced and specific intestinal gastric cancer patients.PREX1 was closely involved in the positive regulation of cell adhesion and positively correlated with TGFβ1-related mediators.Furthermore,TGFβ1 could induce the expression of PREX1 at both the protein and mRNA level.Also,PREX1 could activate the TGFβ1 pathway.The induced PREX1 could increase the migration and invasion activity of gastric cancer cells.CONCLUSION PREX1 is overexpressed in gastric cancer,and the high level of PREX1 predicts poor prognosis.PREX1 is closely associated with TGFβsignaling and promotes the metastasis of gastric cancer cells.
基金supported by Natural Science Foundation of China(No.81001080)Natural Science Foundation of China(No.30901452)
文摘Objective： MicroRNAs （miRNAs） are important regulators that play a key role in tumorigenesis and rumor progression. Transforming growth factor-β1 （TGF-β1） is involved in invasion and metastasis in many tumors. In this study, we investigated the microRNAs （miRNA） profiles altered by TGF-β1 in gastric cancer （GC） cells. Methods： We detected the expression profiles of miRNA by miRNA microarray and quantitative real- time polymerase chain reaction. Migration and invasion, wound-healing assay, prediction of miRNA targets, Western blot and qRT-PCR analysis were carried out to determine the role of one selected miRNA, namely miR-193b, in affecting the biological behaviors of GC BGC823 cells. Results： Among 847 human miRNAs in the microarray, three miRNAs （miR-27a, miR-29b-1 and miR-194） were up-regulated and three （miR-574-3p, miR-193b and miR-130b） were down-regulated in BGC823 cells treated with TGF-β1 compared with control, miR-193b suppressed the invasion and metastasis of GC cells in vivo and in vitro, and down-regulated urokinase-type plasminogen activator （uPA） protein in GC cells. Conclusions： TGF-β1 altered miRNA expression profile in BGC823 cells. Among the altered miRNAs, TGF-β1 induced the down-regulation of miR-193b, which inhibited cell invasion and metastasis in vivo and in vitro, and down-regulated uPA protein in GC cells.
文摘目的探讨胃癌组织中核转录因子-κB(nuclear factor kappa B,NF-κB)、程序性细胞死亡蛋白-1(programmed cell death protein-1,PD-1)、程序性细胞死亡蛋白配体-1(programmed cell death protein ligand 1,PD-L1)的表达及其临床意义。方法选择2021年1月至2023年12月于南阳市第一人民医院治疗的62例胃癌患者手术切除后组织标本及癌旁正常组织标本分别作为胃癌组及癌旁组。62例患者中,男39例,女23例,年龄(61.86±2.31)岁,肿瘤长径(4.92±0.53)cm。采用免疫组织化学染色法检测NF-κB、PD-1、PD-L1表达情况。比较两组NF-κB、PD-1、PD-L1表达阳性率,分析其与胃癌临床病理特征的关系。采用χ^(2)检验。结果胃癌组NF-κB、PD-1、PD-L1表达阳性率高于癌旁组[83.87%(52/62)比33.87%(21/62)、75.81%(47/62)比30.65%(19/62)、80.65%(50/62)比40.32%(25/62)],差异均有统计学意义(χ^(2)=32.008、25.396、21.088,均P<0.05);肌层及浆膜层浸润、有淋巴结转移及Ⅲ+Ⅳ期患者NF-κB表达阳性率高于黏膜及黏膜下层浸润、无淋巴结转移及Ⅰ+Ⅱ期患者[92.68%(38/41)比66.67%(14/21)、94.74(36/38)比66.67%(16/24)、92.31%(36/39)比69.57%(16/23)],差异均有统计学意义(χ^(2)=5.158、6.619、3.978,均P<0.05);肌层及浆膜层浸润、有淋巴结转移及Ⅲ+Ⅳ期患者PD-1表达阳性率高于黏膜及黏膜下层浸润、无淋巴结转移及Ⅰ+Ⅱ期患者[85.37%(35/41)比57.14%(14/21)、89.47%(34/38)比54.17%(13/24)、89.74%(35/39)比52.17%(12/23)],差异均有统计学意义(χ^(2)=6.031、9.998、11.135,均P<0.05);低分化、肌层及浆膜层浸润、有淋巴结转移及Ⅲ+Ⅳ期患者PD-L1表达阳性率高于高中分化、黏膜及黏膜下层浸润、无淋巴结转移及Ⅰ+Ⅱ期患者[96.00%(24/25)比70.27%(26/37)、90.24%(37/41)比61.90%(13/21)、92.11%(35/38)比62.50%(15/24)、94.87%(37/39)比56.52%(13/23)],差异均有统计学意义(χ^(2)=4.787、5.445、6.472、11.286,均P<0.05)。结论胃癌组织中NF-κB、PD-1、PD-L1表达阳性率升高,且NF-κB、PD-1表达与胃癌浸润深度、淋巴结转移及TNM分期有关,PD-L1表达与胃癌分化程度、浸润深度、淋巴结转移及TNM分期有关。
文摘AIM: To investigate the expression of gastrokine 1 (GKN1) in normal gastric mucosa, precancerous lesions and gastric cancer tissues, and to analyse its correlations with tumour site and pathological pattern.
基金Medical science and technology research in Guangdong province(B2018106).
文摘Objective:To study the expression and significance of TNF-transcription factor M1(FoxM1)in bladder cancer and cystitis glandularis(CG).Methods:A total of 30 patients with bladder cancer admitted to our hospital and received surgical treatment from February 2017 to February 2019 were included for the study.During surgery,bladder cancer tissues and normal bladder tissues(tissues more than 5cm away from the cancer tissue center)were collected.Meanwhile,we retained 30 CG tissues from 30 CG patients who received surgical treatment in our hospital at the same time.Bladder cancer cell lines RT4 and BIU87 were cultured and treated with TNF-αat different concentrations(0nM,1nM,5nM,10nM).The expressions of TNF-αand FoxM1 in different bladder tissues were analyzed,and the effects of different concentrations of TNF-αon the expressions of FoxM1 in bladder cancer cell lines and cyclin B1 and cyclin D1 in bladder cancer cell lines were analyzed.Results:The expression levels of TNF-αand FoxM1 in normal bladder,CG and bladder cancer tissues were gradually increased,and univariate analysis of variance showed that the differences between groups were statistically significant(all P<0.05).FoxM1 expression in bladder cancer cell lines treated with TNF-αat concentrations of 0nM,1nM,5nM and 10nM showed a gradual increase trend,and one-way anova showed that the difference between the groups was statistically significant(all P<0.05).After the treatment of bladder cancer cell lines with TNF-αat concentrations of 0nM,1nM,5nM and 10nM,the expression of cyclin B1 and cyclin D1 showed a gradually increasing trend,and one-way anova showed that the difference between groups was statistically significant(all P<0.05).Conclusion:TNF-αmay play a crucial role in the occurrence and development of CG by regulating the expression of transcription factor FoxM1,and then affecting the expression of cyclin B1 and cyclin D1,which is worthy of clinical attention.
