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posted on 2023-03-31, 00:23 authored by Li Zhang, Jianghua Wang, Yongquan Wang, Yiqun Zhang, Patricia Castro, Longjiang Shao, Arun Sreekumar, Nagireddy Putluri, Nilanjan Guha, Saligrama Deepak, Arunkumar Padmanaban, Chad J. Creighton, Michael Ittmann Supplementary Figure 2. MNX1 Protein Overexpression and Knockdown A. Western blot of MNX1 protein levels in two different stable clones of DU145 cells transfected with MNX1 expression vector (OE1 and OE2) versus empty vector controls. β-Actin is a loading control. B. Western blot of MNX1 protein levels in LNCaP cells and stable knockdown cells. LNCaP is untransfected LNCaP and SCR is LNCaP with scrambled vector control. shA, shB and shC are three different MNX1 shRNA transfected stable clones. Note that shB did not knockdown MNX1 and was not used for further experiments. beta-Actin is a loading control.
Funding
Department of Defense
National Cancer Institute
Duncan Cancer Center
CPRIT
Alkek Center for Molecular Discovery
Prostate Cancer Foundation
History
ARTICLE ABSTRACT
Incidence and mortality rates for prostate cancer are higher in African-American (AA) men than in European-American (EA) men, but the biologic basis for this disparity is unclear. We carried out a detailed analysis of gene expression changes in prostate cancer compared with their matched benign tissues in a cohort of AA men and compared them with existing data from EA men. In this manner, we identified MNX1 as a novel oncogene upregulated to a relatively greater degree in prostate cancer from AA men. Androgen and AKT signaling play a central role in the pathogenesis of prostate cancer and we found that both of these signaling pathways increased MNX1 expression. MNX1 in turn upregulated lipid synthesis by stimulating expression of SREBP1 and fatty acid synthetase. Our results define MNX1 as a novel targetable oncogene increased in AA prostate cancer that is associated with aggressive disease. Cancer Res; 76(21); 6290–8. ©2016 AACR.
