BAD overexpression inhibits cell growth and induces apoptosis via mitochondrial-dependent pathway in non-small cell

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Published on: March 30, 2019

Li Jiang1,2, Man Luo1, Dan Liu1

  • 1Department of Respiratory Medicine, West China Hospital, Sichuan University, Chengdu 610041, P.R China.

Cancer Cell International
|June 4, 2013
PubMed
Abstract

Insights

Increased expression of the Bcl-2-associated death promoter (BAD) protein enhances apoptosis and inhibits tumor growth in non-small cell lung cancer (NSCLC). BAD represents a potential therapeutic target for NSCLC interventions.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The Bcl-2-associated death promoter (BAD) protein is a pro-apoptotic factor implicated in human cell apoptosis.
  • BAD has been identified as a prognostic marker in non-small cell lung cancer (NSCLC).

Purpose of the Study:

  • To investigate the functional roles of BAD in non-small cell lung cancer (NSCLC).

Main Methods:

  • BAD was overexpressed in NSCLC cell lines via transfection.
  • In vitro assays assessed cell proliferation, cell cycle, apoptosis, and invasion.
  • In vivo studies evaluated tumorigenicity.
  • Western blotting analyzed Bcl-2 family and apoptosis-related protein expression.

Main Results:

  • BAD overexpression inhibited proliferation and reduced tumorigenicity in specific NSCLC cell lines (H1299, H292, SPC-A1) in vitro and in vivo.
  • Apoptosis was induced in all tested cell types, involving increased mitochondrial cytochrome c and caspase 3 activation.
  • No significant effects on cell cycle distribution or invasion were observed.

Conclusions:

  • Increased BAD expression promotes apoptosis and negatively impacts NSCLC cell proliferation and tumor growth.
  • BAD emerges as a potential therapeutic target for NSCLC treatment.

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