《Induction of Akt activitychemotherapy confers acquired resistance》由会员分享，可在线阅读，更多相关《Induction of Akt activitychemotherapy confers acquired resistance（6页珍藏版）》请在金锄头文库上搜索。
1、Author(s): Huang, WC (Huang, Wei-Chien); Hung, MC (Hung, Mien-Chie)Title: Induction of Akt Activity by Chemotherapy Confers Acquired ResistanceSource: JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION, 108 (3): 180-194 MAR 2009Language: EnglishDocument Type: ReviewAuthor Keywords: Akt; antiapoptosis; canc
2、er; drug resistanceKeyWords 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 P53Abstract: Resistance to c
3、hemotherapy 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 chemor
4、esistant 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,
5、 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
6、 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 Ak
7、t 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); 180-194Addresses: Huang, Wei-Chien; H
8、ung, 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
9、, Dept Mol & Cellular Oncol, Houston, TX 77030 USAReprint Address: Huang, WC, China Med Univ & Hosp, Ctr Mol Med, Taichung 404, Taiwan.E-mail Address: whuangmail.cmu.edu.tw; mhungmdanderson.orgCited References: ACTOR B, 2002, GENE CHROMOSOME CANC, V34, P416.ANDJELKOVIC M, 1997, J BIOL CHEM, V272, P3
10、1515.ANDRE F, 2008, ANN ONCOL, V19, P315, DOI 10.1093/annonc/mdm429.ASHCROFT M, 2002, ONCOGENE, V21, P1955.ASSELIN E, 2001, CANCER RES, V61, P1862.BAJOU K, 1998, NAT MED, V4, P923.BALENDRAN A, 1999, CURR BIOL, V9, P393.BALENDRAN A, 2000, J BIOL CHEM, V275, P20806.BARBONE D, 2008, J BIOL CHEM, V283,
11、P13021, DOI 10.1074/jbc.M709698200.BELLACOSA A, 1995, INT J CANCER, V64, P280.BELYANSKAYA LL, 2005, INT J CANCER, V117, P755, DOI 10.1002/ijc.21242.BERTELSEN BI, 2006, INT J CANCER, V118, P1877, DOI 10.1002/ijc.21461.BEYER BCM, 2006, CANCER, V106, P1026, DOI 10.1002/cncr.21682.BIRCK A, 2000, J INVES
12、T DERMATOL, V114, P277.BOZULIC L, 2008, MOL CELL, V30, P203.BRAUNDULLAEUS RC, 2001, ARTERIOSCL THROM VAS, V21, P1152.BROZOVIC A, 2007, CANCER LETT, V251, P1, DOI 10.1016/j.canlet.2006.10.007.BRUNN GJ, 1996, EMBO J, V15, P5256.BYUN DS, 2003, INT J CANCER, V104, P318, DOI 10.1002/ijc.10962.CAMPBELL IG
13、, 2004, CANCER RES, V64, P7678.CAMPBELL IG, 2005, CLIN CANCER RES 1, V11, P7042, DOI 10.1158/1078-0432.CCR-05-1024.CARDONE MH, 1998, SCIENCE, V282, P1318.CHAZAUD B, 2002, AM J PATHOL, V160, P237.CHEKENYA M, 2008, ONCOGENE, V27, P5182, DOI 10.1038/onc.2008.157.CHENG GZ, 2007, CANCER RES, V67, P1979,
14、DOI 10.1158/0008-5472.CAN-06-1479.CHENG JQ, 1996, P NATL ACAD SCI USA, V93, P3636.CHOI BH, 2008, CANCER LETT, V259, P111, DOI 10.1016/j.canlet.2007.10.003.CLARK AS, 2002, MOL CANCER THER, V1, P707.DATTA SR, 1997, CELL, V91, P231.DELCOMMENNE M, 1998, P NATL ACAD SCI USA, V95, P11211.DELPESO L, 1997,
15、SCIENCE, V278, P687.DEMARCHI F, 2001, J BIOL CHEM, V276, P31738.DEMARCHI F, 2005, DRUG RESIST UPDATE, V8, P359, DOI 10.1016/j.drup.2005.12.001.DU KY, 1998, J BIOL CHEM, V273, P32377.EASTON JB, 2006, ONCOGENE, V25, P6436, DOI 10.1038/sj.onc.1209886.ERMOIAN RP, 2002, CLIN CANCER RES, V8, P1100.ERSTER
16、S, 2004, MOL CELL BIOL, V24, P6728, DOI 10.1128/MCB.24.15.6728-6741.2004.FENG JH, 2004, J BIOL CHEM, V279, P35510, DOI 10.1074/jbc.M404936200.FENG JH, 2004, J BIOL CHEM, V279, P41189, DOI 10.1074/jbc.M406731200.FINGAR DC, 2002, GENE DEV, V16, P1472.FRASER M, 2003, CANCER RES, V63, P7081.FRASER M, 2008, INT J CANCER, V122, P534, DOI 10.1002/ijc.23086.GALLIA GL, 2006, MOL CANCER RE
