Transfection Of Fragile Histidine Triad Gene Induce Apoptosis In Gastric Cancer Cell Line MGC-803 | | Posted on:2004-04-16 | Degree:Master | Type:Thesis | | Country:China | Candidate:M Kong | Full Text:PDF | | GTID:2144360092990759 | Subject:Pathology and pathophysiology | | Abstract/Summary: | PDF Full Text Request | | Stomach cancer is one of the most common human cancers. Inactivation of tumor suppressor gene is a main reason inducing cancerization.Fragile histidine triad (FHIT) gene located in chromosomal region 3p14.2 has been cloned in 1996 by Otha et al. It spans not only the t (3:8) (p14.2; q24) translocation breakpoint found in familial renal cell carcinoma but also the most common human fragile site, FRA3B. Abnormalities in the FHIT gene its expression have been identified in a variety of human cancer cell lines and tumors. FHIT is regarded as a tumor suppressor gene.Researches have demonstrated the correlation between the expression of FHIT protein and incidence and progression of gastric cancer. However, these experiments rarely demonstrated the mechanisms by which the abnormalities in FHIT gene induce the malignant neoplastic transformation of gastric cells.Present studies consider the occurrence of tumor relate to the imbalance between cell proliferation and apoptosis. Some researchers have shown that FHIT gene can induce the apoptosis in esophagus cancer cells. But the results are conflict.Objective: To study FHIT gene effect on apoptosis in gastric cancer cells. ;Methods: FHIT gene was transfected intoMGC-803 cell line (a parent Gastric CancerCell Line devoid of FHTT gene expression, probably a result of neoplastic transformation of the normal gastric cells) by liposome. Western-blot and immunohistochemical assay methods were employed to detect the expression of FHIT. Apoptosis and cell cycle of cell were analyzed by FCMS. Morphological changes were observed by compound and electron microscope.Results: Stable expression of FHIT protein in MGC-803 was obtained. We found the apoptosis cells (32.3% v 12.15%) and percentage of Go/G, cells (64.375% v 49.500)were increased in the FHIT transformed cell line, designated MGC-FHIT (as) compared with the control cell line carrying a plasmid devoid of FHIT, designated MGC-pRcCMV.Conclusion: our data show efficient induction of apoptosis and delay of the cell cycle by the transfection of FHIT gene in gastric cancer cells. These findings present evidences that apoptotic malfunction maybe the reason of neoplastic transformation of FHIT-negative gastric cells and the turbulence of cell cycle maybe a reason of apoptotic malfunction of FHIT-negative gastric cells. | | Keywords/Search Tags: | FHIT gene, gastric cancer, gene transfection, apoptosis,cell cycle,tumor suppressor | PDF Full Text Request | Related items |
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