Expression of alpha CP-4 inhibits cell cycle progression and suppresses tumorigenicity of lung cancer cells

Int J Cancer. 2008 Apr 1;122(7):1512-20. doi: 10.1002/ijc.23236.

Abstract

The protein alpha CP-4 (also known as hnRNP E4) is an RNA binding protein encoded by a gene at 3p21, one of the most common altered regions in lung cancer. It has been proposed that alpha CP-4 may function as a lung tumor suppressor. Lack of alpha CP-4 expression is frequent in highly proliferative lung tumors and correlates with alpha CP-4 allele losses. The aim of this study was to evaluate the effect of alpha CP-4 on the tumorigenic capacity of lung cancer cells. alpha CP-4 expression was induced by transient transfection or stable infection with recombinant retroviruses. Induction of alpha CP-4 expression caused cell cycle arrest in G(2)/M in 3 out of the 7 lung cancer cell lines studied, while no effect on apoptosis was observed. Anchorage-independent growth and invasion capacity of H1299 cells were significantly reduced by alpha CP-4 induction. Tumorigenicity of H1299 cells in nude mice was greatly inhibited by the expression of alpha CP-4. Moreover, induction of alpha CP-4 expression in already established tumors resulted in a sudden growth arrest. Immunocytochemistry analysis of the xenograft tumors revealed an in vivo effect of alpha CP-4 on cell proliferation and no effect on apoptosis. Finally, alpha CP-4 showed a subcellular localization different from alpha CP-4a, a splice variant that does not affect cell proliferation. In conclusion, expression of alpha CP-4 can inhibit proliferation and tumorigenesis of lung cancer cells, both in vivo and in vitro, by delaying the progression of the cell cycle.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / metabolism
  • Adenocarcinoma, Bronchiolo-Alveolar / metabolism
  • Animals
  • Apoptosis*
  • Blotting, Western
  • Carcinoid Tumor / metabolism
  • Carcinoma, Large Cell / metabolism
  • Carcinoma, Non-Small-Cell Lung / genetics
  • Carcinoma, Non-Small-Cell Lung / metabolism*
  • Carcinoma, Non-Small-Cell Lung / physiopathology
  • Carcinoma, Squamous Cell / metabolism
  • Cell Cycle*
  • Chromosomes, Human, Pair 3
  • DNA Damage*
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Immunohistochemistry
  • In Situ Nick-End Labeling
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism*
  • Lung Neoplasms / physiopathology
  • Mice
  • Mice, Nude
  • RNA-Binding Proteins / genetics
  • RNA-Binding Proteins / metabolism*
  • Retroviridae
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transfection
  • Transplantation, Heterologous
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*

Substances

  • PCBP4 protein, human
  • RNA-Binding Proteins
  • Tumor Suppressor Proteins