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[Insulin/PI3K signalling pathway regulates the expression of survivin in liver cancer HepG2 cells]

Ren-hua Guo1, Shi-dai Jin, Jie Cai

  • 1Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China. guorenhua@csco.org.cn

Zhonghua Zhong Liu Za Zhi [Chinese Journal of Oncology]
|January 29, 2009
PubMed
Abstract

Insights

Insulin increases survivin expression in liver cancer cells by activating the PI3K pathway. Blocking this pathway may inhibit survivin, promoting cancer cell death.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Signaling

Background:

  • Survivin is an inhibitor of apoptosis protein crucial in cancer progression.
  • Insulin receptor activation plays a role in hepatocellular carcinoma (HCC) development.
  • Understanding signaling pathways regulating survivin is vital for HCC treatment.

Purpose of the Study:

  • To investigate the effect of insulin on survivin expression in HepG2 HCC cells.
  • To identify the specific signaling pathway involved in insulin-induced survivin regulation.
  • To explore potential therapeutic strategies targeting this pathway.

Main Methods:

  • HepG2 cells were treated with insulin and/or LY294002 (PI3K inhibitor).
  • Survivin mRNA and protein levels were quantified using real-time RT-PCR and Western blot.
  • Dose- and time-dependent effects of insulin on survivin were assessed.

Main Results:

  • Insulin significantly upregulated survivin expression in HepG2 cells in a dose- and time-dependent manner.
  • Pre-treatment with the PI3K inhibitor LY294002 blocked insulin-induced survivin upregulation.
  • Basal survivin expression was low in HepG2 cells without serum supplement.

Conclusions:

  • Insulin promotes survivin expression in HCC cells through the PI3K signaling pathway.
  • Targeting the PI3K/survivin axis could be a therapeutic strategy for HCC.
  • Inhibiting this pathway may enhance apoptosis in hepatocellular carcinoma cells.

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