Basic & Clinical Medicine ›› 2020, Vol. 40 ›› Issue (3): 334-339.

• Original Articles • Previous Articles     Next Articles

Propofol inhibits proliferation, migration and invasion of human lung adenocarcinoma cell lines through down-regulating PKM2

HU Zhi-hui1*, LI Jian-qin2, HAN Lu-jun1, ZHANG Jing1, ZHANG Hong-xin1   

  1. 1. Department of Oncology, the First Hospital of Shijiazhuang City, Shijiazhuang 050011;
    2. Department of Electromyography, Huanghua Municipal People's Hospital, Cangzhou 061300, China
  • Received:2019-04-03 Revised:2019-09-27 Online:2020-03-05 Published:2020-03-02
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Abstract: Objective To investigate the mechanism of propofol on proliferation, migration and invasion of lung adenocarcinoma cells. Methods MTT method was used to detect the inhibition rate or proliferation of A549 and Anip973 human lung adenocarcinoma cell lines treated with propofol (60, 100, 120 μmol/L); The si-NC group (transfected si-NC), the si-PKM2 group (transfected si-PKM2), pcDNA3.1 group (transfected pcDNA3.1), pcDNA3.1-PKM2 group (transfected pcDNA3.1-PKM2), propofol + pcDNA3.1 group (transfected pcDNA3.1 and treated with propofol), propofol + pcDNA3.1-PKM2 group (transfected pcDNA3.1-PKM2 and treated with propofol), all were transfected into Anip973 cells by liposome and treated with propofol; Transwell assay was used to detect cell migration and invasion; RT-qPCR was used to detect the expression of PKM2 mRNA in cells; Western blot was used to detect protein expression of PKM2, E-cadherin, MMP-2, in cells. Results Propofol(0, 60, 100, 120 μmol/L) inhibited the proliferation of human lung adenocarcinoma cells A549 and Anip973 in a concentration-dependent manner. Anip973 cells were more sensitive to propofol, and the optimal concentration was 120 μmol/L; propofol inhibited the proliferation, migration and invasion of Anip973 cells, down-regulated the protein expression of PKM2 and MMP-2, and up-regulated the protein expression of E-cadherin; knockdown of PKM2 has the same inhibition effect as propofol proliferation, migration and invasion, down-regulate the protein expression of MMP-2 and up-regulate the protein expression of E-cadherin of Anip973 cells; over-expression of PKM2 reversed the proliferation, migration and invasion, the effect of protein expression of E-cadherin and MMP-2 of Anip973 cells. Conclusions Propofol inhibits the proliferation, migration and invasion of lung adenocarcinoma cells, and its mechanism is related to down-regulation of PKM2 expression.

Key words: propofol, PKM2, lung adenocarcinoma, proliferation, migration, invasion

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