Author(s): Huang, WC (Huang, Wei-Chien); Hung, MC (Hung, Mien-Chie) Title: Induction of Akt Activity by Chemotherapy Confers Acquired Resistance
Source: JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION, 108 (3): 180-194 MAR 2009
Language: English Document Type: Review
Author Keywords: Akt; antiapoptosis; cancer; drug resistance
KeyWords Plus: NF-KAPPA-B; OVARIAN-CANCER CELLS; PLASMINOGEN-ACTIVATOR INHIBITOR-1; GROWTH-FACTOR RECEPTOR; PROTEIN-KINASE-B; X-LINKED
INHIBITOR; PHOSPHOINOSITIDE 3-KINASE/AKT PATHWAY; CISPLATIN-INDUCED APOPTOSIS; ETOPOSIDE-INDUCED APOPTOSIS; WILD-TYPE P53
Abstract: Resistance to chemotherapy is a major cause of treatment failure in human cancer.
Accumulating evidence has indicated that the acquisition of resistance to chemotherapeutic drugs involves the activation of the PI3K/Akt pathway, modulating Akt activity ill response to chemotherapy has been observed often ill chemoresistant cancers. The potential molecular mechanisms by which chemotherapeutic agents activate the PI3K/Akt pathway arc emerging.
Activation of this pathway evades the cytotoxic effects of chemotherpeutic agents via
regulation of essential cellular functions such as protien synthesis, antiapoptosis, survival and proliferation in cancer flow chemotherapeutic agents induce Akt activation and how activated Akt confers chemoresistance through regulation of signaling networks are discussed in this review. Combining PI3K/Akt inhibitors with standard chemotherapy has been successful in increasing the efficacy of chemotherapeutic agents both in vivo and in vitro. Several small molecules have been developed to specifically target PI3K/Akt and other components of this pathway, which in combination with chemotherapy may be a valid approach mechanisms Of signaling networks for maintenance, of the Akt activity for cell survival. These regulatory mechanisms may limit the efficacy Of PI3K/Akt-targeted therapy; therefore, disruption of these mechanisms may be an effective strategy for development of novel anti-cancer therapies. [J Formos Med Assoc 2009; 108(3); 180-194]
Addresses: [Huang, Wei-Chien; Hung, Mien-Chie] China Med Univ & Hosp, Ctr Mol Med, Taichung 404, Taiwan; [Huang, Wei-Chien; Hung, Mien-Chie] China Med Univ & Hosp, Grad Inst Canc Biol, Taichung 404, Taiwan; [Huang, Wei-Chien; Hung, Mien-Chie] Asia Univ, Dept Biotechnol, Taichung, Taiwan; [Hung, Mien-Chie] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Houston, TX 77030 USA
Reprint Address: Huang, WC, China Med Univ & Hosp, Ctr Mol Med, Taichung 404, Taiwan.
E-mail Address: [email protected]; [email protected]
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Publisher: ELSEVIER SINGAPORE PTE LTD
Publisher Address: 3 KILLINEY ROAD 08-01, WINSLAND HOUSE 1, SINGAPORE, 239519, SINGAPORE
ISSN: 0929-6646
29-char Source Abbrev.: J FORMOS MED ASSOC ISO Source Abbrev.: J. Formos. Med. Assoc.
Source Item Page Count: 15
Subject Category: Medicine, General & Internal ISI Document Delivery No.: 426RH
