Impacts of CyhospitalclinE downstream vimentin on proliferation, invasion and apoptosis of hepatoma HepG2 cell

Objective: To build vimentin (VIM) interference RNA eukaryotic expression vector and observe hepatoma HepG2 cell's capacity of proliferation, apoptosis, changes of its capability of invasion and transfer after CyclinE downstream VIM expression is suppressed. Methods: Firstly, CyclinE gene was knocked out by RNA inference; the changes of HepG2 cell's capacity of proliferation and level of VIM mRNA and protein were observed. Secondly, eukaryotic expression vector of CyclinE downstream VIM interference RNA was built. Thirdly, MTT and Transwell small chamber were used to detect the change of cell's capacity of proliferation and invasion after VIM was silent, and flow cytometry in level of apoptosis. Results: Eukaryotic expression vectors of new biological target VIM interference RNA were built, namely PVIM-1, PVIM-2, PVIM-3 and PVIM-4. CyclinE gene knock-out could prominently suppress HepG2 cell proliferation. Level of VIM mRNA and protein expression was down-regulated after CyclinE-1mRNA was down-regulated. After VIM expression was down-regulated, HepG2 cell's capacity of proliferation and invasion were weakened and apoptosis increased. Conclusion: VIM is involved in proliferation, invasion, leading to more severe cell apoptosis.