p16INK4a inactivation is not required to immortalize human mammary epithelial cells

Brittney Shea Herbert, Woodring E. Wright, Jerry W. Shay

Research output: Contribution to journalArticle

69 Scopus citations

Abstract

Using standard culture conditions, primary human mammary epithelial cells (HMECs) undergo a premature, transient growth arrest termed M0 (mortality stage 0) after 10-15 population doublings in vitro. It has been reported that emergence from this growth arrest by the abrogation of p16INK4a, a cyclin-dependent kinase inhibitor, and expression of the catalytic component of human telomerase (hTERT) are necessary for HMEC immortalization. Here we show that primary HMECs, grown on feeder layers, do not undergo this growth arrest and can be immortalized without abrogating p16. These findings support the concept that the so-called M0 stage represents a cell culture stress-induced growth arrest and that hTERT is sufficient to immortalize HMECs when cultured under adequate conditions.

Original languageEnglish (US)
Pages (from-to)7897-7900
Number of pages4
JournalOncogene
Volume21
Issue number51
DOIs
StatePublished - Nov 7 2002

Keywords

  • Culture
  • Growth arrest
  • Methylation
  • Senescence
  • Telomerase

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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