PT  - JOURNAL ARTICLE
AU  - AHMED, KAZI M.
AU  - CAO, NING
AU  - LI, JIAN JIAN
TI  - HER-2 and NF-κB as the Targets for Therapy-resistant Breast Cancer
DP  - 2006 Nov 01
TA  - Anticancer Research
PG  - 4235--4243
VI  - 26
IP  - 6B
4099  - http://ar.iiarjournals.org/content/26/6B/4235.short
4100  - http://ar.iiarjournals.org/content/26/6B/4235.full
SO  - Anticancer Res2006 Nov 01; 26
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