Overexpression of MTA3 Correlates with Tumor Progression in Non-Small Cell Lung Cancer

PLoS One. 2013 Jun 19;8(6):e66679. doi: 10.1371/journal.pone.0066679. Print 2013.

Abstract

The objective of the current study was to investigate the expression pattern and clinicopathological significance of MTA3 in patients with non-small cell lung cancer (NSCLC). The expression profile of MTA3 in NSCLC tissues and adjacent noncancerous lung tissues was detected by immunohistochemistry. MTA3 was overexpressed in 62 of 108 (57.4%) human lung cancer samples and correlated with p-TNM stage (p<0.0001), nodal metastasis (p = 0.0009) and poor prognosis (p<0.05). In addition, the depletion of MTA3 expression with small interfering RNAs inhibited cell growth and colony formation in the A549 and H157 lung cancer cell lines. Moreover, MTA3 depletion induced cell cycle arrest at the G1/S boundary. Western blotting analysis revealed that the knockdown of MTA3 decreased the protein levels of cyclin A, cyclin D1 and p-Rb. These results indicate that MTA3 plays an important role in NSCLC progression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Cell Line, Tumor
  • Cell Proliferation
  • Cyclins / metabolism
  • Disease Progression
  • Down-Regulation
  • Humans
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology*
  • Lymphatic Metastasis
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*
  • Prognosis
  • Survival Analysis

Substances

  • Cyclins
  • MTA3 protein, human
  • Neoplasm Proteins

Grants and funding

This work was supported by grants from the National Natural Science Foundation of China (No. 30972967) and Specialized Research Fund for the Doctoral Program of Higher Education (No. 20092104110018) and Program for Liaoning Excellent Talents in University. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.