Please use this identifier to cite or link to this item:
|Title:||HOXA1 is required for E-cadherin-dependent anchorage-independent survival of human mammary carcinoma cells|
|Source:||Zhang, X., Emerald, B.S., Mukhina, S., Mohankumar, K.M., Kraemer, A., Yap, A.S., Gluckman, P.D., Lee, K.-O., Lobie, P.E. (2006-03-10). HOXA1 is required for E-cadherin-dependent anchorage-independent survival of human mammary carcinoma cells. Journal of Biological Chemistry 281 (10) : 6471-6481. ScholarBank@NUS Repository. https://doi.org/10.1074/jbc.M512666200|
|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. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.|
|Source Title:||Journal of Biological Chemistry|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Mar 8, 2018
WEB OF SCIENCETM
checked on Feb 6, 2018
checked on Apr 19, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.