Effect and Mechanism of Resveratrol on the Apoptosis of Lung Adenocarcinoma Cell Line A549

Cell Biochem Biophys. 2015 Nov;73(2):527-531. doi: 10.1007/s12013-015-0696-3.

Abstract

Lung adenocarcinoma is the most common subtype of non-small cell lung cancer and the leading cause of cancer death worldwide. In this study, we investigated the effect of resveratrol (Res) on lung adenocarcinoma A549 cells and its potential mechanism. We found after Res treatment, the interspace of A549 cells decreased and granular material increased in the cell nucleus. These changes were remarkably correlated with the increased concentration of Res. Res induces apoptosis in A549 cells and inhibits cell proliferation in a dose-dependent manner. We further showed that after Res treatment, expression of p53, Bax, and cleaved caspase-3 protein was dramatically up-regulated, while expression of Bcl-2 and the ratio of Bcl-2/Bax were down-regulated. Our study demonstrates that Res inhibits proliferation and induces apoptosis of A549 cells through regulation of p53, Bax, Bcl-2, and cleaved caspase-3 expression.

Keywords: Apoptosis; Lung adenocarcinoma; Proliferation; Resveratrol.

MeSH terms

  • A549 Cells
  • Adenocarcinoma
  • Adenocarcinoma of Lung
  • Antineoplastic Agents, Phytogenic / toxicity*
  • Apoptosis / drug effects*
  • Blotting, Western
  • Caspase 3 / metabolism
  • Cell Proliferation / drug effects
  • Humans
  • Lung Neoplasms
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Resveratrol
  • Stilbenes / toxicity*
  • Tumor Suppressor Protein p53 / metabolism
  • bcl-2-Associated X Protein / metabolism

Substances

  • Antineoplastic Agents, Phytogenic
  • Proto-Oncogene Proteins c-bcl-2
  • Stilbenes
  • Tumor Suppressor Protein p53
  • bcl-2-Associated X Protein
  • Caspase 3
  • Resveratrol