PTEN is involved in the signal transduction pathway of contact inhibition in endometrial cells

Kazunori Uegaki, Yasunobu Kanamori, Junzo Kigawa, Wakae Kawaguchi, Ruri Kaneko, Jun Naniwa, Masakuni Takahashi, Muneaki Shimada, Tetsuro Oishi, Hiroaki Itamochi, Naoki Terakawa

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)

Abstract

PTEN is involved in the regulation of normal cellular functions in addition to its well-known role as a tumor suppressor. In the present study, we have shown that stable transfection of the PTEN gene into PTEN-mutated endometrial carcinoma cells leads to contact inhibition accompanied by a decreased level of phosphorylated-Akt (p-Akt) expression, an increase in p27Kip1, and a decrease in β-catenin. PTEN-induced cells with contact inhibition exhibit G0-G1 cell-cycle arrest, and the Ki-67 labeling index is reduced. These changes are canceled by transfection of a double-stranded short-interfering RNA against the PTEN gene. Normal endometrial stromal cells increase their PTEN expression when reaching confluence; this is followed by changes in the expression of Akt-related proteins in the same way as in tumor cells. These results indicate that PTEN, p-Akt, p27, and β-catenin are involved in the signal transduction of contact inhibition and suggest that PTEN may, in part, control the proliferation of endometrial carcinoma cells through the induction of contact inhibition.

Original languageEnglish
Pages (from-to)523-528
Number of pages6
JournalCell and Tissue Research
Volume323
Issue number3
DOIs
Publication statusPublished - 2006 Mar
Externally publishedYes

Keywords

  • Contact inhibition
  • Human endometrial carcinoma cell line
  • PTEN
  • Phosphorylated Akt
  • p27
  • β-catenin

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Histology
  • Cell Biology

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