Paris polyphylla 26 triggers G2/M phase arrest and induces apoptosis in HepG2 cells via inhibition of the Akt signaling pathway

  • J Int Med Res. 2019 Apr;47(4):1685-1695. doi: 10.1177/0300060519826823.
Qiang Li  1 ,  Zifan He  2 ,  Jiming Liu  3 ,  Jianlong Wu  1 ,  Guixiang Tan  4 ,  Jianwei Jiang  2 ,  Zexuan Su  5 ,  Mingrong Cao  1
Affiliations
  • 1. 1 Department of General Surgery, The First Affiliated Hospital, Jinan University, Guangzhou, China.
  • 2. 2 Department of Biochemistry, Medical College, Jinan University, Guangzhou, China.
  • 3. 3 Department of General Surgery, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
  • 4. 4 School of Nursing, Guangdong Pharmaceutical University, Guangzhou, China.
  • 5. 5 Department of Urology, The First Affiliated Hospital, Jinan University, Guangzhou, China.
PMID: 30819018 DOI: 10.1177/0300060519826823
Abstract

Objectives: Paris polyphylla 26 (PP-26) is a monomer purified from Paris polyphylla, which has traditionally been used as an antimicrobial, hemostatic, and Anticancer agent in China. The anti-proliferation effect and underlying molecular mechanism of PP-26 were investigated in vitro.

Methods: The effects of PP-26 on various tumor cells were detected by MTT assay. PP-26-affected cell cycle and cell cycle-related proteins in HepG2 cells were detected by flow cytometry and western blotting, respectively. Apoptosis in response to PP-26 was assessed by Hoechst 33258 staining and flow cytometry. PP-26-affected apoptosis-related proteins and Akt signaling were detected by western blotting. The inhibitory effect of PP-26 on HepG2 cells, when combined with 5-fluorouracil (5-FU), was also assessed.

Results: PP-26 inhibited proliferation of HepG2 cells in a dose-dependent manner by triggering G2/M-phase arrest. Moreover, PP-26 induced Apoptosis of HepG2 cells. Expression levels of Apoptosis proteins Caspase 9, Caspase 3, PARP, Bcl-2, Bcl-xL, and Mcl-1 were downregulated, while the expression level of Apoptosis protein Bax was upregulated. Expression levels of p-Akt, p-GSK-3β, and p-Foxo3 were downregulated. Combination with PP-26 enhanced 5-FU inhibition of HepG2 cell proliferation.

Conclusions: PP-26 triggers G2/M-phase arrest and induces Apoptosis in HepG2 cells via inhibition of the Akt signaling pathway.

Keywords
Akt signaling; Hepatocellular cancer; PP-26; apoptosis; caspase; cell cycle; proliferation.
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