TY - JOUR
AU - 
AB - THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 279, No. 17, Issue of April 23, pp. 17090 –17100, 2004 © 2004 by The American Society for Biochemistry and Molecular Biology, Inc. Printed in U.S.A. JNK Regulates HIPK3 Expression and Promotes Resistance to Fas-mediated Apoptosis in DU 145 Prostate Carcinoma Cells* Received for publication, July 15, 2003, and in revised form, January 28, 2004 Published, JBC Papers in Press, February 6, 2004, DOI 10.1074/jbc.M307629200 James F. Curtin and Thomas G. Cotter‡ From the Tumour Biology Laboratory, Department of Biochemistry, Biosciences Research Institute, University College Cork, Cork, Ireland apeutic regimens do not increase long term survival in patients Elevated endogenous JNK activity and resistance to Fas receptor-mediated apoptosis have recently been im- with prostate cancer (7), and this has been linked to an plicated in progression of prostate cancer and can pro- increased resistance to Fas receptor-mediated apoptosis (8). mote resistance to apoptosis in response to chemother- Hormone-refractory prostate cancer usually displays increased apeutic drugs. In addition, JNK has been demonstrated malignancy, proliferation, and metastatic potential over an- to promote transformation of epithelial cells by increas- drogen-sensitive tumors and can survive in the absence of ing both proliferation and survival. Although numerous androgen. 
TI - JNK Regulates HIPK3 Expression and Promotes Resistance to Fas-mediated Apoptosis in DU 145 Prostate Carcinoma Cells
JF - Journal of Biological Chemistry
DO - 10.1074/jbc.m307629200
DA - 2004-04-01
UR - https://www.deepdyve.com/lp/unpaywall/jnk-regulates-hipk3-expression-and-promotes-resistance-to-fas-mediated-F2Mou9tp0Q
DP - DeepDyve
ER -