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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

[The signal transduction pathway related to hepatocellular carcinoma apoptosis induced by survivin antisense

Tao Chen1, Fu-Zhou Tian, Zhong-Hong Cai

  • 1Center of General Surgery, General Hospital of Chengdu Command, Chengdu 610083 China.

Zhonghua Yi Xue Za Zhi
|June 25, 2003
PubMed
Abstract

Insights

Blocking survivin gene expression with antisense oligonucleotide (ASODN) in hepatocellular carcinoma cells effectively induced apoptosis. This process involves the sequential activation of the p38 mitogen-activated protein kinase (MAPK) and caspase-3 signaling pathway.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Signaling

Background:

  • Survivin is a key protein promoting cancer cell survival.
  • Understanding survivin's role in hepatocellular carcinoma (HCC) is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the effect of blocking survivin gene expression using antisense oligonucleotide (ASODN) in HCC cells.
  • To elucidate the specific signal transduction pathway involved in ASODN-induced apoptosis.

Main Methods:

  • Transfection of SMMC-7721 HCC cells with survivin ASODN using DOTAP liposomal reagent.
  • Assessing survivin expression (mRNA/protein), apoptosis rates (flow cytometry, TUNEL), and the activity of p38MAPK and caspase-3 signaling pathway components.

Main Results:

  • Survivin expression significantly decreased (84.6% protein, 69.7% mRNA) post-ASODN transfection.
  • Apoptosis increased dramatically from 0.70% to 31.15%.
  • ASODN transfection led to sequential activation of p38MAPK and caspase-3, which was inhibited by SB202190.

Conclusions:

  • Survivin ASODN transfection is an effective strategy to induce apoptosis in HCC cells.
  • The p38MAPK-caspase-3 signaling pathway is sequentially activated, mediating ASODN-induced apoptosis in HCC.

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