| Cancer is the most dangerous killer in all the diseases, and lung carcinoma is the most one in all the cancer. So far, the cancerogenic mechanism of lung cancer is not well elucidated. Some growth factors and growth factor receptors have been identified to participate in cancerogenic processes, but the downstream pathways regulated by those growth factor receptors are uncleared. Clarif ing these pathways and genes are essential to understand the cancerogenic process and design medicines.This project is for understanding HCL-G1, which is evidently up-regulated in lung carcinoma cells. G1 belongs to a new gene family, which is highly conserved in most Eukaryotes. We transfected G1-GFP plasmid into Hela cells, and found G1 locating to nucleolus. G1N-terminal-GFP was transfected into Hela cells as the same protocol, but it wasn' t rightly located. The results displayed that G1' s signal peptide in its N-terminal is not enough to get a right location. We examined the growth speed of G1 transfected Hela cells, and found G1 has noticeable plus effect to cell proliferation contrasting to control samples. Flow cytometer results showed that overexpression of G1 promoted G1-S and G2-M transitions. For better understanding the downstream target that G1 regulated, western blot was performed to examine CyclinB\E and CDK2, and CyclinB\E' s expression level weren't distinctly changed. It's likely that G1 regulates in cell-cycle by some other pathways, p53-p21-CDK2 is most understanded so far. We tested some signal pathways related to cell cycle in G1 up-and down-expression Hela cells, and found G1 up-expression down-regulated p53 and p21 level. We identified Gl gene promoter region, and found a 601bp region contributing to G1＞80% expression.
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