Affordable Access

deepdyve-link
Publisher Website

SIRT1 controls cell proliferation by regulating contact inhibition.

Authors
  • Cho, Elizabeth H1
  • Dai, Yan2
  • 1 Cancer Center, Hematology Oncology Section, Department of Medicine, Boston University School of Medicine, 72 East Concord Street, L913, Boston, MA 02118, United States. , (United States)
  • 2 Cancer Center, Hematology Oncology Section, Department of Medicine, Boston University School of Medicine, 72 East Concord Street, L913, Boston, MA 02118, United States. Electronic address: [email protected] , (United States)
Type
Published Article
Journal
Biochemical and Biophysical Research Communications
Publisher
Elsevier
Publication Date
Sep 16, 2016
Volume
478
Issue
2
Pages
868–872
Identifiers
DOI: 10.1016/j.bbrc.2016.08.041
PMID: 27514448
Source
Medline
Keywords
License
Unknown

Abstract

Contact inhibition keeps cell proliferation in check and serves as a built-in protection against cancer development by arresting cell division upon cell-cell contact. Yet the complete mechanism behind this anti-cancer process remains largely unclear. Here we present SIRT1 as a novel regulator of contact inhibition. SIRT1 performs a wide variety of functions in biological processes, but its involvement in contact inhibition has not been explored to date. We used NIH3T3 cells, which are sensitive to contact inhibition, and H460 and DU145 cancer cells, which lack contact inhibition, to investigate the relationship between SIRT1 and contact inhibition. We show that SIRT1 overexpression in NIH3T3 cells overcomes contact inhibition while SIRT1 knockdown in cancer cells restores their lost contact inhibition. Moreover, we demonstrate that p27 protein expression is controlled by SIRT1 in contact inhibition. Overall, our findings underline the critical role of SIRT1 in contact inhibition and suggest SIRT1 inhibition as a potential strategy to suppress cancer cell growth by restoring contact inhibition.

Report this publication

Statistics

Seen <100 times