Rho A protein pathway in the DLC1 gene regulation in human colon cancer HT29 cell cycle and its mechanism.docVIP

 PAGE \* MERGEFORMAT 14 Rho A protein pathway in the DLC1 gene regulation in human colon cancer HT29 cell cycle and its mechanism Of: Ping-Ping Wu, Su Yun, Jin governance, Wu Peng, Xu Jiajia, Pei-Lin Huang [Abstract] Objective: To investigate the Rho A protein pathway in the DLC 1 (frequently deleted in liver cancer 1) gene regulation of human colon cancer HT29 cell cycle and its mechanism. METHODS: pcDNA3.1 DLC1 plasmid, liposome transfected HT29 cells, stable cell line selection; pull down method of Rho A protein activity; real-time quantitative PCR detection of cell cycle-related proteins Cyclin D1, p21 expression changes; cell cycle distribution by flow cytometry. Results: wild-type human colon carcinoma HT29 cells DLC 1 gene expression was negative, obtained by transfection of stable cell lines DLC 1. with wild-type and no-load group compared with HT29 cells, transfected cells decreased activity of Rho A protein; Cyclin D1 downregulation, p21 expression increased; G1 phase and increase the number of apoptotic cells, and G2 phase cells decreased. CONCLUSION: Transfection of DLC 1 gene cause human colon cancer HT29 cells reduced activity of Rho A protein, which may by Cyclin D1, p21 regulation of the expression of the cell cycle G1 phase arrest and induction of apoptosis, while reducing the number of prophase cells, cell proliferation inhibition. [Keywords:] liver cancer gene to 1; Rho A protein; Cyclin D1 gene; p21 gene; cell cycle; HT29 cell line Liver cancer gene to 1 (frequently deleted in liver cancer 1, DLC 1), located on human chromosome 8p21.3 22, is a new candidate tumor suppressor gene .1998 Yuan et al [1] First, from the primary hepatocellular carcinoma separated and that the gene change is one of an early event in HCC. Subsequently, it was discovered that DLC 1 gene expression decreased in most tumors or absent, in vivo experiments also demonstrate DLC 1 protein can inhibit the growth of various tumor cells and tumorigenicity [23]. Th