E2F2 induction in related to cell proliferation and poor prognosis in non-small cell lung carcinoma

Int J Clin Exp Pathol. 2015 Sep 1;8(9):10545-54. eCollection 2015.

Abstract

E2F transcription factors regulate a wide range of biological processes, including cell cycle, apoptosis and DNA damage response. In the present study, we examined whether E2F2 is related to the poor prognosis of NSCLC and its role in progress of NSCLC. Firstly, we analyzed 86 NSCLC samples by immunohistochemistry and found that E2F2 expression was markedly increased in 62.8% (54/86) of all samples compared with the normal tissues. Further study showed that E2F2 expression was closely associated with clinical stage (P = 0.039) and tumor size (P = 0.045). Furthermore, Kaplan-Meier analysis indicated that high Bad expression was significantly correlated to overall survival (P = 0.045) but not disease-free survival (P = 0.288). In addition, our results showed that knockdown E2F2 expression could reduce cell viability and colony formation in NSCLC cells. The results in our study for the first time revealed that E2F2 act as an activator in tumor progress of NSCLC and could become a promising marker for the prognosis of patients with NSCLC.

Keywords: E2F2; NSCLC; prognosis; proliferation; survival.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Biomarkers, Tumor / metabolism
  • Blotting, Western
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / mortality
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Cell Line, Tumor
  • Cell Proliferation
  • Disease-Free Survival
  • E2F2 Transcription Factor / biosynthesis*
  • Female
  • Humans
  • Immunohistochemistry
  • Kaplan-Meier Estimate
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / mortality
  • Lung Neoplasms / pathology*
  • Male
  • Middle Aged
  • Prognosis
  • RNA, Small Interfering
  • Transfection

Substances

  • Biomarkers, Tumor
  • E2F2 Transcription Factor
  • E2F2 protein, human
  • RNA, Small Interfering