Transcription factor EGR-1 inhibits growth of hepatocellular carcinoma and esophageal carcinoma cell

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:ustbyjp
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AIM:The transcription factor EGR-1(early growth responsegene-1)plays an important role in cell growth,differentiation and development.It has identified that EGR-1has significant transformation suppression activity in someneoplasms,such as fibrosarcoma,breast carcinoma.Thisexperiment was designed to investigate the role of egr-1 inthe cancerous process of hepatocellular carcinoma(HCC)and esophageal carcinoma(EC),and then to appraise theeffects of EGR-1 on the growth of these tumor cells.METHODS:Firstly,the transcription and expression of egr-1in HCC and EC,paracancerous tissues and their normalcounterpart parts were detected by in situ hybridization andimmunohistochemistry,with normal human breast andmouse brain tissues as positive controls.Egr-1 gene wasthen transfected into HCC(HHCC,SMMC7721)and EC(ECa109)cell lines in which no egr-1 transcription andexpression were present.The cell growth speed,FCM cellcycle,plate clone formation and tumorigenicity in nude micewere observed and the controls were the cell linestransfected with vector only.RESULTS:Little or no egr-1 transcription and expressionwere detected in HCC,EC and normal liver tissues.Theexpression of egr-1 were found higher in hepatocellularparacancerous tissue(transcription level P=0.000;expression level P=0.143,probably because fewer innumber of cases)and dysplastic tissue of esophagealcancer(transcription level P=0.000;expression level P=0.00l).The growth rate of egr-1-transfected HHCC(HCC cellline)cells and ECa109(EC cell line)cells was much slowerthan that of the controls.The proportion of S phase cell,clone formation and tumorigenicity were significantly lowerthan these of the controls’(decreased 45.5 % in HHCC cellsand 34.1% in ECal09 cells;46.6% and41.8%;80.4% and72.6 % respectively).There were no obvious differencesbetween SMMC7721(HCC)egr-1-transfected cells and thecontrols with regard to the above items.CONCLUSION:The decreased expression of egr-1 might play a role in the dysregulation of normal growth in the cancerous process of HCC and EC. Egr-1 gen of transfected HHCCand ECa109 cells showed obvious suppression of the cell growth and malignant phenotypes, but no suppression in SMMC7721(HCC cell line)cells. AIM: The transcription factor EGR-1 (early growth responsegene-1) plays an important role in cell growth, differentiation and development. It has been identified that EGR-1 significant transformation suppression activity in some neoplasms, such as fibrosarcoma, breast carcinoma. Hisexperiment was designed to investigate the role of egr-1 inthe cancerous process of hepatocellular carcinoma (HCC) and esophageal carcinoma (EC), and then to appraise the effects of EGR-1 on the growth of these tumor cells. METHODS: Firstly, the transcription and expression of egr-1 in HCC and EC, paracancerous tissues and their normalcounterpart parts were detected by in situ hybridization and immunohistochemistry, with normal human breast and mouse brain tissues as positive controls. Egr-1 gene wasthen transfected into HCC (HHCC, SMMC7721) and EC (ECa 109 ) cell lines in which no egr-1 transcription were expressed in the cell growth speed, FCM cellcycle, plate clone formation and tumorigenicity in nude mice were observed and the c ontrols were the cell linestransfected with vector only .RESULTS: Little or no egr-1 transcription and expressionwere detected in HCC, EC and normal liver tissues. Theexpression of egr-1 were found higher in hepatocellularparacancerous tissue (transcription level P = 0.000; expression level Probably due to fewer innumber of cases) and dysplastic tissue of esophageal cancer (transcription level P = 0.000; expression level P = 0.001). The growth rate of egr- 1-transfected HHCC (HCC cellline) cells and ECa 109 cell line) cells was much slowererthan that that of the controls.The proportion of S phase cell, clone formation and tumorigenicity were significantly lowererthan these of the controls’ (decreased 45.5% in HHCC cells and 34.1% in ECal09 cells; 46.6% and 41.8% ; 80.4% and72.6% respectively). Where no obvious differences between SMMC7721 (HCC) egr-1-transfected cells and the controls with regard to the above items. CONCLUSION: The decreased expression of egr-1 might play a role in the dysregulation of normalGrowth in the cancerous process of HCC and EC. Egr-1 gen of transfected HHCC and ECa109 cells showed obvious suppression of the cell growth and malignant phenotypes, but no suppression in SMMC7721 (HCC cell line) cells.
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