Effects Of MACC1 In Proliferation And Migration Of Esophageal Carcinoma Cells And Its Mechanism

[Objective]To detect the effects of MACC1 in proliferation and migration of esophageal carcinoma cells and its possible mechanism.[Methods]1.The expression of MACC1 in EC 10、 EC9706、 TE13、 EC1 and normal esophageal epithelial cell lines HEEpiC were measured by RT-PCR and Western blot. TE13 (low expression of MACC1) and EC 109 (high expression of MACC1) cell line was used as an ideal model for studying the role of MACC1 in tumorigenesis.2. Adenoviral construct encoding the MACC1 gene (Ad-MACC1) was used to infect TE13 cells for increasing the expression of MACCland MACC1 siRNA transfection EC 109 cells for reducing the expression of MACC1 and their expression were analyzed by by Western blot.3. The TE13 and EC109 was treatment by Ad-MACCl and MACC1 siRNA respectively. The proliferation effect of MACClwas analyzed by MTT assay and and its effect on the cell cycle was analyzed by fow cytometry. The cell migration effect of MACC1 was examined by scrape-migration assay. Colony formation in soft agarose was performed to analyze the effect of MACC1 on the anchorage-independent growth of the cells.4. The expression of proliferating cell nuclear antigen (PCNA) and c-MET were dedetect Using Western blot.[Results]1. The expression of MACCl was higher in EC9706 and Eca109 cells than normal esophageal epithelial cell lines HEEpiC,but it is lowe in TE13 and EC1 cells.2. We have successfully constructed Ad-MACC1 and MACC1 siRNA.Western blotting showed that TE13 was the most sensitive to adenoviral infection and EC 109 to MACC1 siRNA.Therefore, we chose the TE13 and EC 109 cells as an ideal model for following studying.3. The results showed that the Ad-MACC1 caused a significant increase in the number of live cells and migration in TE13 cells. However, proliferation and migration of EC 109 cells was obviously inhibited by MACC1 siRNA transfection.4. The expression of PCNA and c-MET gene and protein was significantly increased in TE13 cells which infect Ad-MACC1,while in EC 109 cell was low expression because of MACC1 siRNA transfection.[Conclusion]The expression of MACCl is higher in EC9706 and Eca109 cell lines than TE13 and EC1 cells.Its high expression can promote cell proliferation and migration, on the contrary, inhibited esophageal cancer cell proliferation and invasion.These data indicate that the MACC1 promote the biology activity of esophageal cancer cells. Our results strongly suggest that MACC1 is a potential cancer factor.The mechanism of MACC1 promote Eca-109 cells invasion and migrating perhaps through the regulation downstream gene c-MET expression level.