HOXA1 is required for E-cadherin-dependent anchorage-independent survival of human mammary carcinoma cells

Xin Zhang, B. Starling Emerald, Svetlana Mukhina, Kumarasamypet M. Mohankumar, Astrid Kraemer, Alpha S. Yap, Peter D. Gluckman, Kok Onn Lee, Peter E. Lobie

Research output: Contribution to journalArticlepeer-review

30 Citations (Scopus)

Abstract

Forced expression of HOXA1 is sufficient to stimulate oncogenic transformation of immortalized human mammary epithelial cells and subsequent tumor formation. We report here that the expression and transcriptional activity of HOXA1 are increased in mammary carcinoma cells at full confluence. This confluence-dependent expression of HOXA1 was abrogated by incubation of cells with EGTA to produce loss of intercellular contact and rescued by extracellular addition of Ca2+. Increased HOXA1 expression at full confluence was prevented by an E-cadherin function-blocking antibody and attachment of non-confluent cells to a substrate by homophilic ligation of E-cadherin increased HOXA1 expression. E-cadherin-directed signaling increased HOXA1 expression through Rac1. Increased HOXA1 expression consequent to E-cadherin-activated signaling decreased apoptotic cell death and was required for E-cadherin-dependent anchorage-independent proliferation of human mammary carcinoma cells. HOXA1 is therefore a downstream effector of E-cadherin-directed signaling required for anchorage-independent proliferation of mammary carcinoma cells.

Original languageEnglish
Pages (from-to)6471-6481
Number of pages11
JournalJournal of Biological Chemistry
Volume281
Issue number10
DOIs
Publication statusPublished - Mar 10 2006
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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