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The role of tazarotene-induced gene 1 in carcinogenesis:is it a tumor suppressor gene or an oncogene?
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作者 CHUN-HUA WANG LU-KAI WANG +1 位作者 RONG-YAUN SHYU FU-MING TSAI 《BIOCELL》 SCIE 2024年第9期1285-1297,共13页
Tazarotene-induced gene 1(TIG1)is induced by a derivative of vitamin A and is known to regulate many important biological processes and control the development of cancer.TIG1 is widely expressed in various tissues;yet... Tazarotene-induced gene 1(TIG1)is induced by a derivative of vitamin A and is known to regulate many important biological processes and control the development of cancer.TIG1 is widely expressed in various tissues;yet in many cancer tissues,it is not expressed because of the methylation of its promoter.Additionally,the expression of TIG1 in cancer cells inhibits their growth and invasion,suggesting that TIG1 acts as a tumor suppressor gene.However,in some cancers,poor prognosis is associated with TIG1 expression,indicating its protumor growth characteristics,especially in promoting the invasion of inflammatory breast cancer cells.This review comprehensively summarizes the roles of the TIG1 gene in cancer development and details the mechanisms through which TIG1 regulates cancer development,with the aim of understanding its various roles in cancer development. 展开更多
关键词 Tazarotene-induced gene 1 Retinoic acid receptor responder protein 1 Tumor suppressor gene ONCOGENE
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Aberrant Methylation in CpG Islands of pl5 and pl6 Tumor Suppressor Genes in Pancreatic Cancer Tissue 被引量:3
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作者 董科 李波 +3 位作者 覃杨 刘建余 李承志 孙芝琳 《The Chinese-German Journal of Clinical Oncology》 CAS 2005年第4期213-217,共5页
Objective: To detect the aberrant methylation patterns in the CpG islands of p16 and p15 tumor suppressor genes, and to analyze its correlation with pancreatic carcinogenesis and with clinicopathological characterist... Objective: To detect the aberrant methylation patterns in the CpG islands of p16 and p15 tumor suppressor genes, and to analyze its correlation with pancreatic carcinogenesis and with clinicopathological characteristics of patients with pancreatic cancer (PC). Methods: The methylation-specific polymerase chain reaction (MSP) method was used to monitor methylation patterns in the CpG islands of p15 and p16 genes from 29 cases of PC and 3 cases of chronic pancreatitis (CP) paraffin-embedded tissue, as well as 2 cases of normal liver tissues and 12 cases of normal blood samples. Results: p15 and p16 genes were detected to show unmethylation patterns and no amplification using methylation-specific primers in control group. The aberrant methylation rates of p16 in carcinoma tissue and adjacent noncarcinoma tissue were 37.9% (11 of 29 cases) and 34.5% (10 of 29 cases) respectively. Of the 11 aberrant methylated samples, 5 showed complete methylation and 6 hemimethylation. The methylation rates of p15 gene in carcinoma tissue and adjacent noncarcinoma tissue were 27.5% (8/29) and 24.4% (7/29) respectively. Of the 8 aberrant methylated samples, 3 showed complete methylation and 5 hemimethylation. In 6 PC samples, aberrant methylation in CpG islands of both p15 and p16 genes existed simultaneously. The aberrant methylation patterns in CpG islands of p15 and p16 genes had no close correlation with the clinicopathological characteristics (age, sex, smoking, volume of primary tumor, differentiation, clinical stage and histological classification) of the patients with PC (P〉0.05). Conclusion: The aberrant methylation in CpG islands of p15 and p16 genes could be regarded as an early molecular event in PC and had no close correlation with the clinicopathological characteristics of the patients with PC. 展开更多
关键词 METHYLATION suppressor gene pancreatic cancer
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Mapping of metastasis suppressor genes for prostate cancer by microcell-mediated chromosome transfer 被引量:2
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作者 Tomohiko ICHIKAWA Shigeru HOSOKI +9 位作者 Hiroyoshi SUZUKI Koichiro AKAKURA Tatsuo IGARASHI Yuzo FURUYA Mitsuo OSHIMURA Carrie W.RINKER-SCHAEFFER Naoki NIHEI J.Carl BARRETT John T.ISAACS Haruo ITO 《Asian Journal of Andrology》 SCIE CAS CSCD 2000年第3期167-171,共5页
Aim:To identify the metastasis suppressor genes for prostate cancer.Methods:A copy of human chromosomeswas introduced into the highly metastatic Dunning R-3327 rat prostate cancer cells by the use of microcell-mediate... Aim:To identify the metastasis suppressor genes for prostate cancer.Methods:A copy of human chromosomeswas introduced into the highly metastatic Dunning R-3327 rat prostate cancer cells by the use of microcell-mediatedchromosome transfer.Relationships between the size of human chromosomes introduced into microcell hybrid clonesand the number of lung metastases produced by the clones were analyzed to determine which part of human chromo-somes contained the metastasis suppressor gene(s)for prostate cancer.To determine portions of human chromosomesintroduced,G-banding chromosomal analysis,fluorescence in sim hybridization analysis,and polymerase chain reac-tion analysis were performed.Results:Each of microcell hybrid clones containing human chromosomes 7,8,10,11,12,or 17 showed decreased ability to metastasize to the lung without any loss of tumorigenicity.This demonstratesthat these human chromosomes contain metastasis suppressor genes for prostate cancer.Spontaneous deletion of portionsof human chromosomes was observed in the human chromosome 7,10,11,12,and 17 studies.In the human chromo-some 8 study,irradiated microcell-mediated chromosome transfer was performed to enrich chromosomal arm deletionsof human chromosome 8.Molecular and cytogenetic analyses of microcell hybrid clones demonstrated that metastasissuppressor genes on human chromosomes were located on 7q21-22,7q31.2-32,8p21-12,10q11-22,11p13-11.2,12p11-q13,12q24-ter,and 17pter-q23.KAII and MKK4/SEKI were identified as metastasis suppressor genes from11p11.2 and 17p12,respectively.Conclusion:This assay system is useful to identify metastasis suppressor gene(s)for prostate cancer. 展开更多
关键词 prostate cancer METASTASIS metastasis suppressor gene CHROMOSOME
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CHROMOSOME 3 MAY HARBOR MULTIPLE TUMOR SUPPRESSOR GENES ASSOCIATED WITH PRIMARY GLIOBLASTOMA MULTIFORME
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作者 胡杰 江澄川 +3 位作者 吴浩强 彭颂先 唐婉君 陈商群 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2002年第3期183-186,共4页
Objective: To investigate whether deletion of chromosome 3 is involved in the carcinogenesis of primary glioblastoma multiforme (GBM) and to localize the possible common deletion region in the aforementioned chromosom... Objective: To investigate whether deletion of chromosome 3 is involved in the carcinogenesis of primary glioblastoma multiforme (GBM) and to localize the possible common deletion region in the aforementioned chromosome. Methods: PCR based microsatellite polymorphism analyses were performed to detect loss of heterozygosity (LOH). Twenty-three loci on chromosome 3 were examined in 20 cases of GBM. Fluorescence-labeled primers and Perkin Elmer 377 DNA Sequencer were applied. Results: 50% informative cases of GBM displayed LOH on chromosome 3. 50% of informative cases displayed LOH on 3q and 35% on 3p. 25.6% of informative loci showed LOH in our series, in which frequent LOH were observed in the chromosomal region from loci D3S1614 (42.9%) to D3S1565 (35.3%) on 3q24–27 and at loci D3S1569 (35.3%) on 3q22–23 and D3S1289 (33.3%) on 3p14.1–14.3. Conclusion: Loss of genetic material on chromosome 3 may play an important part in the tumorigenesis of GBM. The chromosomal regions from loci D3S1614 to D3S1565 on 3q24–27 and at loci D3S1569 on 3q22–23 and D3S1289 on 3p14.1–14.3 are potential sites for novel tumor suppressor genes associated with GBM. 展开更多
关键词 Loss of heterozygosity GLIOBLASTOMA Tumor suppressor gene Chromosome 3
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CHROMOSOME 17P MAY HARBOR MULTIPLE TUMOR SUPPRESSOR GENES ASSOCIATED WITH PRIMARY GLIOBLASTOMA MULTIFORME
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作者 胡杰 江澄川 +2 位作者 吴浩强 彭颂先 唐婉君 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2002年第1期60-63,共4页
Objective: To investigate whether deletion of chromosome 17 is involved in the carcinogenesis of primary glioblastoma multiforme and to localize the possible common deletion region in the aforementioned chromosome. Me... Objective: To investigate whether deletion of chromosome 17 is involved in the carcinogenesis of primary glioblastoma multiforme and to localize the possible common deletion region in the aforementioned chromosome. Methods: Polymerase chain reaction-based microsatellite analysis was used to assess loss of heterozygosity (LOH) on chromosome 17 in 20 primary glioblastoma multiforme (GBM). Fifteen fluorescent dye-labeled polymorphic markers were used. Results: Thirteen of twenty (65%) GBM displayed LOH on at least one marker of chromosome 17p. Two tumors showed either LOH or non-informativeness on all markers tested. The most frequent LOH was observed at loci including D17s799 (53.3%), D17s1852 (53.8%), D17s938 (63.20/o), D17s831 (55.6%). The loci D17s831 (on 17p13) and D17s799–D17s1852 (17p11.2–p12) are distal and proximal to p53 respectively. The frequencies of LOH at all loci examined on chromosome 17q were relatively low (<30%). None of informative loci exhibited microsatellite instability in this study. Conclusion: Loss of genetic material on chromosome 17p may play an important role in the pathogenesis of GBM. Besides the well-known TSG p53 on 17p, other unknown TSCs associated with GBM may be present on the chromosomal regions 17p13 and 17p11.2–p12, which are distal and proximal to p53 respectively. 展开更多
关键词 Loss of heterozygosity GLIOBLASTOMA Tumor suppressor genes Chromosome 17
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Are there tumor suppressor genes on chromosome 4p in sporadic colorectal carcinoma?
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作者 Hai-Tao Zheng Li-Xin Jiang +5 位作者 Zhong-Chuan Lv Da-Peng Li Chong-Zhi Zhou Jian-Jun Gao Lin He Zhi-Hai Peng 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第1期90-94,共5页
AIM: To study the candidate tumor suppressor genes (TSG) on chromosome 4p by detecting the high frequency of loss of heterozygosity (LOH) in sporadic colorectal carcinoma in Chinese patients.METHODS: Seven fluorescent... AIM: To study the candidate tumor suppressor genes (TSG) on chromosome 4p by detecting the high frequency of loss of heterozygosity (LOH) in sporadic colorectal carcinoma in Chinese patients.METHODS: Seven fluorescent labeled polymorphic microsatellite markers were analyzed in 83 cases of colorectal carcinoma and matched normal tissue DNA by PCR. PCR products were eletrophoresed on an ABI 377 DNA sequencer. Genescan 3.7 and Genotype 3.7 software were used for LOH scanning and analysis. The same procedure was performed by the other six microsatellite markers spanning D4S3013 locus to make further detailed deletion mapping. Comparison between LOH frequency and clinicopathological factors was performed by χ2 test.RESULTS: Data were collected from all informative loci. The average LOH frequency on 4p was 24.25%, and 42.3% and 35.62% on D4S405 and D4S3013 locus, respectively. Adjacent markers of D4S3013 displayed a low LOH frequency (< 30%) by detailed deletion mapping. Significant opposite difference was observed between LOH frequency and tumor diameter on D4S412 and D4S1546 locus (0% vs 16.67%, P = 0.041; 54.55% vs 11.11%, P = 0.034, respectively). On D4S403 locus, LOH was significantly associated with tumor gross pattern (11.11%, 0, 33.33%, P = 0.030). No relationship was detected on other loci compared with clinicopathologial features.CONCLUSION: By deletion mapping, two obvious high frequency LOH regions spanning D4S3013 (4p15.2) and D4S405 (4p14) locus are detected. Candidate TSG, which is involved in carcinogenesis and progression of sporadic colorectal carcinoma on chromosome 4p, may be located between D4S3017 and D4S2933 (about 1.7 cm). 展开更多
关键词 Loss of heterozygosity Colorectal carcinoma Chromosome 4p Tumor suppressor gene
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Lecithin-cholesterol acyltransferase is a potential tumor suppressor and predictive marker for hepatocellular carcinoma metastasis
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作者 Yan Li Li-Na Jiang +7 位作者 Bo-Kang Zhao Mei-Ling Li Yi-Yun Jiang Yi-Si Liu Shu-Hong Liu Li Zhu Xin Ye Jing-Min Zhao 《World Journal of Gastrointestinal Oncology》 SCIE 2024年第8期3651-3671,共21页
BACKGROUND Hepatocellular carcinoma(HCC)is a major cause of cancer mortality worldwide,and metastasis is the main cause of early recurrence and poor prognosis.However,the mechanism of metastasis remains poorly underst... BACKGROUND Hepatocellular carcinoma(HCC)is a major cause of cancer mortality worldwide,and metastasis is the main cause of early recurrence and poor prognosis.However,the mechanism of metastasis remains poorly understood.AIM To determine the possible mechanism affecting HCC metastasis and provide a possible theoretical basis for HCC treatment.METHODS The candidate molecule lecithin-cholesterol acyltransferase(LCAT)was screened by gene microarray and bioinformatics analysis.The expression levels of LCAT in clinical cohort samples was detected by quantitative realtime polymerase chain reaction and western blotting.The proliferation,migration,invasion and tumor-forming ability were measured by Cell Counting Kit-8,Transwell cell migration,invasion,and clonal formation assays,respectively.Tumor formation was detected in nude mice after LCAT gene knockdown or overexpression.The immunohistochemistry for Ki67,E-cadherin,N-cadherin,matrix metalloproteinase 9 and vascular endothelial growth factor were performed in liver tissues to assess the effect of LCAT on HCC.Gene set enrichment analysis(GSEA)on various gene signatures were analyzed with GSEA version 3.0.Three machine-learning algorithms(random forest,support vector machine,and logistic regression)were applied to predict HCC metastasis in The Cancer Genome Atlas and GEO databases.RESULTS LCAT was identified as a novel gene relating to HCC metastasis by using gene microarray in HCC tissues.LCAT was significantly downregulated in HCC tissues,which is correlated with recurrence,metastasis and poor outcome of HCC patients.Functional analysis indicated that LCAT inhibited HCC cell proliferation,migration and invasion both in vitro and in vivo.Clinicopathological data showed that LCAT was negatively associated with HCC size and metastasis(HCC size≤3 cm vs 3-9 cm,P<0.001;3-9 cm vs>9 cm,P<0.01;metastatic-free HCC vs extrahepatic metastatic HCC,P<0.05).LCAT suppressed the growth,migration and invasion of HCC cell lines via PI3K/AKT/mTOR signaling.Our results indicated that the logistic regression model based on LCAT,TNM stage and the serum level of α-fetoprotein in HCC patients could effectively predict high metastatic risk HCC patients.CONCLUSION LCAT is downregulated at translational and protein levels in HCC and might inhibit tumor metastasis via attenuating PI3K/AKT/mTOR signaling.LCAT is a prognostic marker and potential therapeutic target for HCC. 展开更多
关键词 Lecithin-cholesterol acyltransferase Tumor suppressor gene Hepatocellular carcinoma PI3K/AKT/MTOR Predicting model
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Cloning and Expression Analysis of a Human Putative Tumor Suppressor Gene Homologue from Rice
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作者 葛晓春 宗晖 +3 位作者 詹树萱 陈继超 孙崇荣 曹凯鸣 《Acta Botanica Sinica》 CSCD 2002年第5期562-566,共5页
A gene homologous to the human Putative tumor suppressor gone QM, designated OSQM1, was isolated from rice (Oryza sativa L.) genomic DNA library using through homology screening. It contained 4 exons and 3 introns, en... A gene homologous to the human Putative tumor suppressor gone QM, designated OSQM1, was isolated from rice (Oryza sativa L.) genomic DNA library using through homology screening. It contained 4 exons and 3 introns, encoding a protein of 219 amino acids with 46 basic amino acids, leading to a high isoelectric point of 11.02. Homology search showed that this gene existed in eukaryotes and highly conserved throughout eukaryotes, suggesting an essential role of this gene. Northern Not analysis showed that it was expressed in various rice organs, but at lower level in developing flower and callus tissue than in other vegetative organs. Its expression levels in roots and leaves were influenced by different environmental factors. 展开更多
关键词 tumor suppressor gene QM EUKARYOTES
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Inactivation of RASSF1A, the tumor suppressor gene at 3p21.3 in extrahepatic cholangiocarcinoma 被引量:22
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作者 Yong-JunChen Qi-BinTang Shen-QuanZou 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第9期1333-1338,共6页
AIM: To evaluate the genetic and epigenetic inactivation mechanism of the RASSF1A tumor suppressor gene at 3p21.3 in extrahepatic cholangiocarcinoma. METHODS: RT-PCR was used to investigate the transcriptional express... AIM: To evaluate the genetic and epigenetic inactivation mechanism of the RASSF1A tumor suppressor gene at 3p21.3 in extrahepatic cholangiocarcinoma. METHODS: RT-PCR was used to investigate the transcriptional expressing and re-expression of RASSFIA. RASSFIA mutation was analyzed with SSCP and selective sequencing. PCR was performed to detect the loss of heterozygosity (LOH) at the region of chromosome 3p21.3. Genomic DNA were modificated bisulfite and the frequency of methylation of CpG islands in RASSFIA promoter were evaluated by methylation specific PCR (MS-PCR). RESULTS: In all 48 samples and one cell lines of extrahepatic cholangiocarcinoma, the RASSFIA mutation is rare (6.12%, 3/49), 33 samples (68.75%) and QBC-939 cell lines (X2= 14.270, P= 0.001<0.01) showed RASSFIA express inactivation with LOH at microsatellite loci D3S4604. Among these 33 samples and QBC-939, 28 of 33 (84.85%) tumor samples and 1 cell lines were methylated for majority of 16 CpGs, the average frequency is 73.42%. CONCLUSION: The data we present suggest that RASSFIA which we have been searching for at 3p21.3 may be one of the key tumor suppressor gene and play an important role in the pathogenesis of extrahepatic cholangiocarcinoma, and the promoter methylation and allelic loss are the major mechanism for inactivation of RASSFIA. 展开更多
关键词 RASSF1A Tumor suppressor gene CHOLANGIOCARCINOMA
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Aberrant expression of genes and proteins in pterygium and their implications in the pathogenesis 被引量:10
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作者 Qing-Yang Feng Zi-Xuan Hu +1 位作者 Xi-Ling Song Hong-Wei Pan 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2017年第6期973-981,共9页
Pterygium is a common ocular surface disease induced by a variety of factors. The exact pathogenesis of pterygium remains unclear. Numbers of genes and proteins are discovered in pterygium and they function differentl... Pterygium is a common ocular surface disease induced by a variety of factors. The exact pathogenesis of pterygium remains unclear. Numbers of genes and proteins are discovered in pterygium and they function differently in the occurrence and development of this disease. We searched the Web of Science and PubMed throughout history for literatures about the subject. The keywords we used contain pterygium, gene, protein, angiogenesis, fibrosis, proliferation, inflammation, pathogenesis and therapy. In this review, we summarize the aberrant expression of a range of genes and proteins in pterygium compared with normal conjunctiva or cornea, including growth factors, matrix metalloproteinases and tissue inhibitors of mefalloproteinases, interleukins, tumor suppressor genes, proliferation related proteins, apoptosis related proteins, cell adhesion molecules, extracellular matrix proteins, heat shock proteins and tight junction proteins. We illustrate their possible mechanisms in the pathogenesis of pterygium as well as the related intervention based on them for pterygium therapy. 展开更多
关键词 PTERYGIUM growth factors MATRIXMETALLOPROTEINASES tissue inhibitors of metalloproteinases INTERLEUKINS tumor suppressor genes proliferation andapoptosis cell adhesion molecules extmcellular matrix proteins
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Inactivation of the tumor suppressor Krüppel-like factor 6 (KLF6) by mutation or decreased expression in hepatocellular carcinomas 被引量:5
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作者 PAN Xiu-cheng CHEN Zhi CHEN Feng CHEN Xiao-hong JIN Han-yin XU Xiao-yan 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2006年第10期830-836,共7页
Background and aim: The Krueppel-like transcription factor KLF6 is a novel tumor-suppressor gene. It was inactivated in human prostate cancer and other tumors tissue, as the result of frequent mutation and loss of he... Background and aim: The Krueppel-like transcription factor KLF6 is a novel tumor-suppressor gene. It was inactivated in human prostate cancer and other tumors tissue, as the result of frequent mutation and loss of heterozygosity (LOH). However, there is no data reporting the levels of KLF6 both mRNA and protein in hepatocellular carcinomas (HCCs). We therefore detected mutations and expression of KLF6 in HCC tissues and further observed the effect of it on cell growth in HCC cell lines. Methods: We analyzed the exon-2 ofKLF6 gene by direct DNA sequencing, and detected the expression of KLF6 by RT-PCR and Western blot in 23 HCC tissues and corresponding nontumorous tissues. Loss of growth suppressive effect of the HCC-derived KLF6 mutant was characterized by in vitro growth curves plotted, flow cytometry and Western blotting. Results: KLF6 mutations were found in 2 of 23 HCC tissues and one of mutations was missense. Expression ofKLF6 mRNA or protein was down-regulated in 8 (34.7%) or 9 (39.1%) of 23 HCC tissues. Wild-type KLF6 (wtKLF6) inhibited cellular proliferation and prolonged G1 -S transition by inducing the expression of p21WAF 1 following stable transfection into cultured HepG2 cells, but tumor-derived KLF6 mutant (mKLF6) had no effects. Conclusion: Our findings suggest that KLF6 may be involved in pathogenesis of HCC. 展开更多
关键词 Tumor suppressor gene Krueppel-like factor 6 (KLF6) MUTATION Gene expression Hepatocellular carcinoma
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Aberrant methylation of the 3q25 tumor suppressor gene PTX3 in human esophageal squamous cell carcinoma 被引量:3
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作者 Jun-Xiong Wang Yuan-Long He +2 位作者 Sheng-Tao Zhu Shuo Yang Shu-Tian Zhang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第37期4225-4230,共6页
AIM:To identify the novel methylation-silenced gene pentraxin 3(PTX3) in esophageal squamous cell carcinoma(ESCC).METHODS:PTX3 mRNA expression was examined in six human ESCC cell lines,one human immortalized normal es... AIM:To identify the novel methylation-silenced gene pentraxin 3(PTX3) in esophageal squamous cell carcinoma(ESCC).METHODS:PTX3 mRNA expression was examined in six human ESCC cell lines,one human immortalized normal esophageal epithelial cell line,primary ESCC tumor tissue,and paired adjacent nontumor tissue using reverse transcription polymerase chain reaction(RTPCR).Semi-quantitative immunohistochemistry was used to examine cellular localisation and protein levels.Methylation specific PCR and bisulphite genomic sequencing were employed to investigate the methylation of the candidate gene.RESULTS:In the majority of ESCC cell lines,we found that PTX3 expression was down-regulated due to gene promoter hypermethylation,which was further confirmed by bisulphite genomic sequencing.Demethylation treatment with 5-aza-2'-deoxycytidine restored PTX3 mRNA expression in ESCC cell lines.Methylation was more common in tumor tissues(85%) than in adjacent nontumor tissues(25%)(P < 0.01).CONCLUSION:PTX3 is down-regulated through promoter hypermethylation in ESCC,and could potentially serve as a biomarker of ESCC. 展开更多
关键词 Tumor suppressor gene Pentraxin 3 MICROARRAY DNA methylation Esophageal squamous cell carcinoma
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Tumor suppress genes screening analysis on 4q in sporadic colorectal carcinoma 被引量:1
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作者 Li-Xin Jiang Jie Xu +5 位作者 Zhao-Wen Wang Da-Peng Li Zhi-Hai Peng Jian-Jun Gao Lin He Hai-Tao Zheng 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第36期5606-5611,共6页
AIM: To search candidate tumor suppressor genes (TSGs) on chromosome 4q through detecting high loss of heterozygosity (LOH) regions in sporadic colorectal carcinoma in Chinese patients. METHODS: Thirteen fluorescent l... AIM: To search candidate tumor suppressor genes (TSGs) on chromosome 4q through detecting high loss of heterozygosity (LOH) regions in sporadic colorectal carcinoma in Chinese patients. METHODS: Thirteen fluorescent labeled polymorphic microsatellite markers were analyzed in 83 cases of colorectal carcinoma and matched normal tissue DNA by polymerase chain reaction (PCR). PCR products were eletrophoresed on an ABI 377 DNA sequencer. Genescan 3.7 and Genotype 3.7 software were used for LOH scanning and analysis. Comparison between LOH frequency and clinicopathological factors were performed by χ2 test. RESULTS: Data were collected on all informative loci. The average LOH frequency on 4q was 28.56%. The D4S2915 locus showed highest LOH frequency (36.17%). Two obvious deletion regions were detected: one between D4S3000 and D4S2915 locus (4q12-21.1), another flanked by D4S407 and D4S2939 locus (4q25-31.1). None case showed complete deletion of 4q, most cases displayed interstitial deletion pattern solely. Furthermore, compared with clinicopathological features, a significant relationship was observed between LOH frequencies on D4S3018locus. In tumors larger than 5 cm in diameter, LOH frequency was significantly higher than tumors that were less than 5 cm (56% vs 13.79%, P = 0.01). On D4S1534 locus, LOH was significantly associated with liver metastasis (80% vs 17.25%, P = 0.012). No relationship was detected on other locus compared with clinicopathologial features. CONCLUSION: By high resolution deletion mapping, two high frequency regions of LOH (4q12-21.1 and 4q25-31.1) were detected, which may contribute to locate TSGs on chromosome 4q involved in carcinogenesis and progression of sporadic colorectal carcinoma. 展开更多
关键词 Loss of heterozygosity Colorectal carcinoma Chromosome 4q Tumor suppressor gene
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Role of p53 suppression in the pathogenesis of hepatocellular carcinoma 被引量:2
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作者 Heena B Choudhary Satish K Mandlik Deepa S Mandlik 《World Journal of Gastrointestinal Pathophysiology》 2023年第3期46-70,共25页
In the world,hepatocellular carcinoma(HCC)is among the top 10 most prevalent malignancies.HCC formation has indeed been linked to numerous etiological factors,including alcohol usage,hepatitis viruses and liver cirrho... In the world,hepatocellular carcinoma(HCC)is among the top 10 most prevalent malignancies.HCC formation has indeed been linked to numerous etiological factors,including alcohol usage,hepatitis viruses and liver cirrhosis.Among the most prevalent defects in a wide range of tumours,notably HCC,is the silencing of the p53 tumour suppressor gene.The control of the cell cycle and the preservation of gene function are both critically important functions of p53.In order to pinpoint the core mechanisms of HCC and find more efficient treatments,molecular research employing HCC tissues has been the main focus.Stimulated p53 triggers necessary reactions that achieve cell cycle arrest,genetic stability,DNA repair and the elimination of DNA-damaged cells’responses to biological stressors(like oncogenes or DNA damage).To the contrary hand,the oncogene protein of the murine double minute 2(MDM2)is a significant biological inhibitor of p53.MDM2 causes p53 protein degradation,which in turn adversely controls p53 function.Despite carrying wt-p53,the majority of HCCs show abnormalities in the p53-expressed apoptotic pathway.High p53 in-vivo expression might have two clinical impacts on HCC:(1)Increased levels of exogenous p53 protein cause tumour cells to undergo apoptosis by preventing cell growth through a number of biological pathways;and(2)Exogenous p53 makes HCC susceptible to various anticancer drugs.This review describes the functions and primary mechanisms of p53 in pathological mechanism,chemoresistance and therapeutic mechanisms of HCC. 展开更多
关键词 Hepatocellular carcinoma P53 Tumour suppressor gene Murine double minute 2 CHEMORESISTANCE
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ISOLATION OF TUMOR DIFERENTIALLY EXPRESSED GENES BY MIXING PROBES LIBRARY SCREEN
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作者 余鹰 朱诗国 +4 位作者 张必成 周鸣 李桂源 沈守荣 张晓梅 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2001年第2期79-82,共4页
Objective: This study was designed to clone candidate tumor suppressor genes down-expressed in Nasopharyngeal Carcinoma (NPC). Methods: Differentially expressed cDNA fragments (AF152605 and AF091517) were labeled by P... Objective: This study was designed to clone candidate tumor suppressor genes down-expressed in Nasopharyngeal Carcinoma (NPC). Methods: Differentially expressed cDNA fragments (AF152605 and AF091517) were labeled by PCR, and Northern blot was used to confirmed transcript length of these genes. Skeleton muscle cDNA library was screened with PCR-labeled probe mixture. Results: 23 positive independent and overlapping positive clones were obtained. By sequencing the positive clones directly, three novel genes (Genbank accession number: AF179285, AF170307 and AF194971), with transcripts of 2.1 Kb, 1.1 Kb and 1.4 Kb respectively, were isolated successfully. Conclusions: Library screening using PCR-labeled probes mixture is an efficient method to get full-length cDNA from multi-cDNA fragment simultaneously and quickly. 展开更多
关键词 Nasopharyngeal carcinoma cDNA library scrren Tumor suppressor gene Gene cloning
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Interaction of Human Genes WT1 and CML28 in Leukemic Cells
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作者 毛霞 张冰 +2 位作者 刘龙龙 白雪玲 张东华 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2013年第1期37-42,共6页
The molecular pathogenesis of leukemia is poorly understood. Earlier studies have shown both Wilms' tumor 1 suppressor gene (WT1) and CML28 abnormally expressed in malignant diseases of the hematopoietic system and... The molecular pathogenesis of leukemia is poorly understood. Earlier studies have shown both Wilms' tumor 1 suppressor gene (WT1) and CML28 abnormally expressed in malignant diseases of the hematopoietic system and WT1 played an important role in leukemogenesis. However, the rela- tionship between molecular CML28 and WT1 has not been reported. Here we described the use of small interfering RNA (siRNA) against WT1 and CML28 in leukemic cell line K562 to examine the interac- tion between CML28 and WT1. WT1 and CML28 gene expression in transfected K562 cells was de- tected by using RQ-PCR and Western blotting. K562 cells transfected with WTI-siRNA could greatly decrease both mRNA and protein expression levels of WT1 and CML28. In contrast, CML28-siRNA did not exert effect on WT1. Further, subcellular co-localization assay showed that the two proteins could co-localize in the cytoplasm of K562 cells, but WT1/CML28 complexes were not detected by us- ing immunoprecipitation. It was suggested that there exists the relationship between CML28 and WT1. CML28 may be a downstream target molecule of WT1 and regulated by WT1, which will provide im- portant clues for further study on the role of CML28 and WT1 in leukemic cells. 展开更多
关键词 Wilms' tumor 1 suppressor gene CML28 K562 SIRNA
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Expression of the Tumor Metastatic Suppressor Gene in Mouse Melanoma Model: Inverse Association to Metastatic Potential
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作者 孟力 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 1998年第1期28-32,36,共6页
Data obtained in experimental cutaneous melanomas have suggested that the nm23 gene may function as a metastasis suppressor gene. The nm23 level in 8 human cutaneous melanoma cell lines and 2 murine melanoma cell line... Data obtained in experimental cutaneous melanomas have suggested that the nm23 gene may function as a metastasis suppressor gene. The nm23 level in 8 human cutaneous melanoma cell lines and 2 murine melanoma cell lines were examined. Each melanoma cell line was transplanted subcutaneously into the flank of nude mice, and the metastatic behavior was evaluated by counting lung tumor fool and by determining host survival time. It was found that expression of 'm23 mRNA in human melanomas is correlated closely with reduced metastatic behavior in experimental animals and may serve as a sensitive prognostic indicator of malignancy and survival in patients with melanomas. 展开更多
关键词 human melanoma tumor metastatic suppressor gene PROGNOSIS
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Overexpression of a novel gene , Cms1, can rescue the growth arrest of a Saccharomyces cerevisiae mcm10 suppressor
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作者 WangJW WuJR 《Cell Research》 SCIE CAS CSCD 2001年第4期285-291,共7页
MCM10 protein is an essential replication factor involved in the initiation of DNA replication. A mcm10 mutant (mcm10-1) of budding yeast shows a growth arrest at 37 degrees C. In the present work, we have isolated a ... MCM10 protein is an essential replication factor involved in the initiation of DNA replication. A mcm10 mutant (mcm10-1) of budding yeast shows a growth arrest at 37 degrees C. In the present work, we have isolated a mcm10-1 suppressor strain, which grows at 37 degrees C. Interestingly, this mcm10-1 suppressor undergoes cell cycle arrest at 14 degrees C. A novel gene, YLR003c, is identified by high-copy complementation of this suppressor. We called it as Cms1 (Complementation of Mcm 10 Suppressor). Furthermore, the experiments of transformation show that cells of mcm10-1 suppressor with high-copy plasmid but not low-copy plasmid grow at 14 degrees C, indicating that overexpression of Cms1 can rescue the growth arrest of this mcm10 suppressor at non-permissive temperature. These results suggest that CMS1 protein may functionally interact with MCM10 protein and play a role in the regulation of DNA replication and cell cycle control. 展开更多
关键词 genes suppressor Amino Acid Sequence Cell Cycle Proteins Cell Division Cloning Molecular genes Fungal Molecular Sequence Data Research Support Non-U.S. Gov't Saccharomyces cerevisiae Saccharomyces cerevisiae Proteins Sequence Alignment Sequence Analysis Protein
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Potential effect of hepatitis C Virus non-structural protein 4B on liver carcinogenesis
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作者 Xia Chen Changping Li Zhongqiong Wang Guanghong DU 《Journal of Nanjing Medical University》 2006年第6期387-391,共5页
Objective:To investigate the effect of hepatitis C virus non-structural protein 4B(HCV NS4B) on c-Myc, P53, ras gene expression" and apoptosis in hepatic cells and study the possible role that NS4B played in the c... Objective:To investigate the effect of hepatitis C virus non-structural protein 4B(HCV NS4B) on c-Myc, P53, ras gene expression" and apoptosis in hepatic cells and study the possible role that NS4B played in the carcinogenesis of heparoma. Methods: The recombinant plasmid(PCXN2-NS4B, PCXN2-P53) and the empty, vector were transfected or co-transfected into Chang liver cells with liposome. Screening was performed with G418. Plasmid mRNA was detected by RT-PCR. The pro rein expressions of c-Myc and ras genes were analyzed by immunocytochemistry. The expressions of wild-type P53 (wtp53) gene were detected by in situ hybridization. TUNEL(flow cytometry) was used for assessing the rate of apoptosis. Results:No expression of c-Myc gene was found in PCXN2 group. The expression of c-Myc gene in NS4B group was 21.3% + 1.2%. The ex pression of ras gene in PCXN2 group was lower than that in NS4B group. Compared with PCXN2 group, the expression of P53 mRNA was not promoted or inhibited in NS4B group. But the expression of P53 mRNA in NS4B-P53 group was lower than that in P53 group. In PCXN2, NS4B, P53 and NS4B-P53 group, the rates of apoptosis were 17.02% ± 1.24%, 11.94% ± 2.24%, 25.84% ± 3.49% and 18.34% ± 1.55% respectively. Conclusion :HCV NS4B induces the expression of c-Myc and ras gene. HCV NS4B may play a role in the inhibition of cell death through P53-dependent manner. Results from this study suggested that HCV NS4B might contribute to the viral carcinogenesis. 展开更多
关键词 non-structural protein 4B tumor suppressor gene ONCOGENE APOPTOSIS
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Modeling human brain rhabdoid tumor by inactivating tumor suppressor genes in induced pluripotent stem cells
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作者 Timothy Hua Yu Xue +3 位作者 Drishty B.Sarker Sonia Kiran Yan Li Qing-Xiang Amy Sang 《Bioactive Materials》 SCIE CSCD 2024年第1期136-150,共15页
Atypical teratoid/rhabdoid tumor(ATRT)is a rare childhood malignancy that originates in the central nervous system.Over ninety-five percent of ATRT patients have biallelic inactivation of the tumor suppressor gene SMA... Atypical teratoid/rhabdoid tumor(ATRT)is a rare childhood malignancy that originates in the central nervous system.Over ninety-five percent of ATRT patients have biallelic inactivation of the tumor suppressor gene SMARCB1.ATRT has no standard treatment,and a major limiting factor in therapeutic development is the lack of reliable ATRT models.We employed CRISPR/Cas9 gene-editing technology to knock out SMARCB1 and TP53 genes in human episomal induced pluripotent stem cells(Epi-iPSCs),followed by brief neural induction,to generate an ATRT-like model.The dual knockout Epi-iPSCs retained their stemness with the capacity to differentiate into three germ layers.High expression of OCT4 and NANOG in neurally induced knockout spheroids was comparable to that in two ATRT cell lines.Beta-catenin protein expression was higher in SMARCB1-deficient cells and spheroids than in normal Epi-iPSC-derived spheroids.Nucleophosmin,Osteopontin,and Ki-67 proteins were also expressed by the SMARCB1-deficient spheroids.In summary,the tumor model resembled embryonal features of ATRT and expressed ATRT biomarkers at mRNA and protein levels.Ribociclib,PTC-209,and the combination of clofilium tosylate and pazopanib decreased the viability of the ATRT-like cells.This disease modeling scheme may enable the establishment of individualized tumor models with patient-specific mutations and facilitate high-throughput drug testing. 展开更多
关键词 Atypical teratoid/rhabdoid tumor Human induced pluripotent stem cells CRISPR/Cas9 gene editing Tumor suppressor genes SMARCB1 Brain tumor modeling
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