Objective To investigate the effect of caveolion-1 on the growth and proliferation in human breastcancer MCF7 cell in vitro and in vivo and approach its mechanisms. Methods The plasmid pCI-neo-cav-1 and its corres-ponding empty vector （pCI-neo） were transfected into MCF7 cell line. The expressions of caveolin-1 and vascular endoth-elial growth factor （VEGF） in transfectants were subsequently confirmed by Western blot analysis. A pair of monoclonal cell lines， MCF7/cav-1 and MCF7/vec， were chose for future studies. The colony formation ability of tumor cells was detected by anchorage-independent growth assay. Xenograft tumor models in nude mice were established. Immunohisto-chemistry was used to characterize Ki-67 and VEGF levels in the tumors tissues. Results Caveolin-1 expression was up-regulated in the MCF7/cav-1 cell as compared with the MCF7/vec cell （P＜0.01） and the MCF7 cell （P＜0.01）. Caveolin-1 overexpression markedly reduced the capacity of the cells to form colonies in soft agar （P＜0.01）. Compared with the MCF7/vec cell， VEGF protein expression reduced in the MCF7/cav-1 cell （P＜0.01）. In vivo experiments in nude mice， the overexpression of caveolin-1 resulted in significant growth inhibition of the xenograft breast tumors. The Ki-67 staining was weak and the VEGF staining was negative by immunohistochemistry that indicated the caveolin-1 inhibited the proliferation in human breast cancer MCF7 cell. Conclusion The caveolin-1 might inhibit the growth and proliferation in human breast cancer MCF7 cell through suppressing activation of VEGF signaling pathway.
ObjectiveTo investigate the effect and mechanism of caveolion-1 on the growth and proliferation of human pancreatic carcinoma cell Panc1, in vitro. MethodsThe plasmid pCI-neo-cav-1 and its corresponding empty vector (pCI-neo) were transfected into Panc1 cell line (study group and control group, respectively). Expressions of caveolin-1, Akt, and Aktphosphate (p-Akt) were determined in transfectants by Western blot analysis. The cell growth curve was drawn and the double time was calculated in each group, and the cell cycle was analyzed by flow cytometry. The colony formation ability of tumor cells was detected by anchorageindependent growth assay. ResultsCaveolin-1 expression was up-regulated (Plt;0.01) and the growth of Panc1 cell was inhibited significantly (Plt;0.01) in the study group comparing with the control group. Caveolin-1 overexpression inhibited proliferation of Panc1 cell by arresting the cell cycle in the G0/G1 phase (Plt;0.05), the rate of S phase in the study group was lower than that of the control group (Plt;0.01). Proliferation index of the study group was also lower than that of the control group (Plt;0.01). Caveolin-1 overexpression reduced the capacity of the cells to form colonies in soft agar (Plt;0.01). p-Akt protein was reduced in the study group as compared with the control group (Plt;0.05). ConclusionCaveolin-1 can function as a cancer suppressor through inhibiting the activation of PI3K/Akt signaling pathway in Panc1 cell.