RT Journal Article
SR Electronic
T1 HER-2 and NF-κB as the Targets for Therapy-resistant Breast Cancer
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 4235
OP 4243
VO 26
IS 6B
A1 AHMED, KAZI M.
A1 CAO, NING
A1 LI, JIAN JIAN
YR 2006
UL http://ar.iiarjournals.org/content/26/6B/4235.abstract
AB HER-2 (also called ErbB2 or Neu) tyrosine kinase, one of the four members of ErbB receptor family (ErbB1, i.e., EGFR, ErbB2, ErbB3 and ErbB4), plays a critical role in the control of diverse cellular functions involved in differentiation, proliferation, migration and cell survival via multiple signal transduction pathways. Overexpression of HER-2, observed in HER-2-positive breast cancer patients, is believed to cause the tumor resistance to an array of anti-cancer agents and poor prognosis. Although HER-2 antibodies have shown growth inhibitory effects, more efficient molecular targets against HER-2-mediated tumor resistance need to be developed. The molecular mechanisms underlying HER-2-mediated tumor resistance, especially the connections between HER-2 and therapy-resistant signaling networks, need to be further investigated. NF-κB, a key stress transcription factor that can initiate a pro-survival network, was found to be activated in many cancer cells overexpressing HER-2 and to be responsible for the radiation resistance in HER-2 transfected breast cancer cells. Recent findings in literature and data from this laboratory suggest a possible co-operation between HER-2 and NF-κB in signaling tumor resistance to radiotherapy. This review will discuss the mechanisms of HER-2 mediated NF-κB signaling pathway and potential target for therapeutic intervention. Copyright© 2006 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved