Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

E2F3a is a transcription factor that has been shown to be overexpressed in liver cancer tissues. To characterize the function of E2F3a in hepatocellular carcinoma (HCC), effects of ectopic overexpression of E2F3a on cell cycle, apoptosis, and gene expression of HepG2 cells were studied. E2F3a significantly enhances the apoptotic rate of HepG2 cells by 33% but only has minor effects on cell proliferation. By using microarray analyses, we identified 162 target genes (160 upregulated and 2 downregulated) of the E2F3a. Differential expression of 11 genes was further confirmed by real-time PCR. Eight of these 11 genes, including XAF1, CEACAM1, STAT1, ATF3, TNFSF10, KLF6, CLDN1, and TAP1, were confirmed to be upregulated by more than twofold. Functional enrichments of differentially expressed genes retrieved 21 apoptosis-related genes and 32 transcriptional regulation-related genes. These results suggest that E2F3a induces apoptosis in HepG2 cells and plays important roles in regulating transcription. Finally, positive correlation was found between E2F3a and CEACAM1 mRNA levels in clinically well-differentiated human HCC specimens.
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PMID:Characterization of E2F3a function in HepG2 liver cancer cells. 2080 51

X-linked inhibitor of apoptosis (XIAP)-associated factor 1 (XAF1), a XIAP-binding protein, is a tumor suppressor gene. XAF1 was silent or expressed lowly in most human malignant tumors. However, the role of XAF1 in hepatocellular carcinoma (HCC) remains unknown. In this study, we investigated the effect of XAF1 on tumor growth and angiogenesis in hepatocellular cancer cells. Our results showed that XAF1 expression was lower in HCC cell lines SMMC-7721, Hep G2 and BEL-7404 and liver cancer tissues than that in paired non-cancer liver tissues. Adenovirus-mediated XAF1 expression (Ad5/F35-XAF1) significantly inhibited cell proliferation and induced apoptosis in HCC cells in dose- and time- dependent manners. Infection of Ad5/F35-XAF1 induced cleavage of caspase -3, -8, -9 and PARP in HCC cells. Furthermore, Ad5/F35-XAF1 treatment significantly suppressed tumor growth in a xenograft model of liver cancer cells. Western Blot and immunohistochemistry staining showed that Ad5/F35-XAF1 treatment suppressed expression of vascular endothelial growth factor (VEGF), which is associated with tumor angiogenesis, in cancer cells and xenograft tumor tissues. Moreover, Ad5/F35-XAF1 treatment prolonged the survival of tumor-bearing mice. Our results demonstrate that XAF1 inhibits tumor growth by inducing apoptosis and inhibiting tumor angiogenesis. XAF1 may be a promising target for liver cancer treatment.
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PMID:Tumor suppressor XAF1 induces apoptosis, inhibits angiogenesis and inhibits tumor growth in hepatocellular carcinoma. 2498 Aug 21