In:
Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. LB-189-LB-189
Abstract:
Metastasis is responsible for over 90% of cancer deaths. However, biochemical and molecular mechanisms that regulate tumor progression to metastatic phenotype are still poorly understood, especially the control of survival and proliferation of metastatic cells. Kinases play key roles in regulation of many cellular processes. Here we employed an unbiased RNAi in vitro screen against human kinases and a focused cDNA in vivo screen to identify kinases that have novel roles in metastasis. Beta adrenergic receptor kinase 2 (BARK2, ADRBK2, GRK3) was one of the kinases we discovered to have a novel role in cancer progression through this work. It was essential for survival and proliferation of metastatic cells in vitro and in vivo. Moreover, it was also sufficient to promote primary prostate tumor growth and metastasis upon exogenous expression in poorly metastatic cells in mouse xenograft models. Mechanistically, we found that GRK3 functions at least in part through regulating several angiogenic factors and stimulating angiogenesis. Furthermore, GRK3 was found to be overexpressed in human prostate cancers, especially in metastasis. Taken together, these data suggest that GRK3 plays an important role in prostate cancer progression and metastasis. Citation Format: Nanping Ai, Mohit Hulsurkar, Lars Akslen, Randolph Watnick, Ed Harlow, Wenliang Li. GRK3 is essential for metastatic cells and promotes prostate cancer progression. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-189. doi:10.1158/1538-7445.AM2014-LB-189
Type of Medium:
Online Resource
ISSN:
0008-5472
,
1538-7445
DOI:
10.1158/1538-7445.AM2014-LB-189
Language:
English
Publisher:
American Association for Cancer Research (AACR)
Publication Date:
2014
detail.hit.zdb_id:
2036785-5
detail.hit.zdb_id:
1432-1
detail.hit.zdb_id:
410466-3
Permalink