Abstract 4970: The role of POU5F1B in prostate cancer

2014 
Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA POU5F1B is the one of the pseudogenes of POU5F1 (also known as Oct3, Oct4) with protein-coding potential. It is localized on chromosome 8q24.21, inside of the 1.2 Mb “gene desert” between the FAM84B and the c-MYC gene, which is closely associated with prostate cancer risk. Recent studies shown that POU5F1B, but not POU5F1, is expressed in prostate tissue and is overexpressed in prostatic carcinoma, compared to normal prostatic tissue surrounding the carcinoma. However, the role of POU5F1B in prostate cancer is still unknown. Through in silico analysis of dataset HG-U95A, we found that POU5F1B expression is increased in prostate tumor and markedly increased in metastatic tumors. Western blot analysis revealed a marked increase in POU5F1B expression in prostate cancer cells when compared to non-tumorigenic RWPE-1 cells. To study the role of POU5F1B in prostate cancer, we cloned POU5F1B from prostate cancer cells, sequenced the amplicons, and found several polymorphism. We made pCDH-myc-POU5F1B constructs and expressed POU5F1B in prostate cancer cell lines LNCaP, DU145, and PC-3. Prostate cancer cell lines that ectopically overexpress POU5F1B form dramatically fewer cell-cell junctions and exhibit significantly increased invasiveness in vitro. Further, we found that E-Cadherin expression is downregulated in DU145-POU5F1B cells. Methylation of the E- Cadherin locus is increased in DU145-POU5F1B cells and methyltransferase inhibitors can partially restore E-Cadherin expression. These data collectively suggest an important role of POU5F1B in prostate tumor progression and metastasis. Citation Format: Hongmei Jiang, Man-Tzu Wang, Daotai Nie. The role of POU5F1B in prostate cancer. [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 4970. doi:10.1158/1538-7445.AM2014-4970
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