Newswire (Published: Tuesday, April 25, 2017, Received: Friday, April 21, 2017, 5:51:51 AM CDT)
Word Count: 520
Findings in Prostate Cancer Reported from University of North Carolina (Up-Regulation of Follistatin-Like 1 By the Androgen Receptor and Melanoma Antigen-A11 in Prostate Cancer)
By a News Reporter-Staff News Editor at Cancer Weekly -- A new study on Oncology - Prostate Cancer is now available. According to news reporting originating from Chapel Hill, North Carolina, by NewsRx correspondents, research stated, "High affinity androgen binding to the androgen receptor (AR) activates genes required for male sex differentiation and promotes the development and progression of prostate cancer. Human AR transcriptional activity involves interactions with coregulatory proteins that include primate-specific melanoma antigen-A11 (MAGE-A11), a coactivator that increases AR transcriptional activity during prostate cancer progression to castrationresistant/recurrent prostate cancer (CRPC)."
Our news editors obtained a quote from the research from the University of North Carolina, "Microarray analysis and quantitative RT-PCR were performed to identify androgen-regulated MAGE-A11-dependent genes in LAPC-4 prostate cancer cells after lentivirus shRNA knockdown of MAGE-A11. Chromatin immunoprecipitation was used to assess androgen-dependent AR recruitment, and immunocytochemistry to localize an androgen-dependent protein in prostate cancer cells and tissue and in the CWR22 human prostate cancer xenograft. Microarray analysis of androgen-treated LAPC-4 prostate cancer cells indicated follistatin-like 1 (FSTL1) is up-regulated by MAGE-A11. Androgen-dependent up-regulation of FSTL1 was inhibited in LAPC-4 cells by lentivirus shRNA knockdown of AR or MAGE-A11. Chromatin immunoprecipitation demonstrated AR recruitment to intron 10 of the FSTL1 gene that contains a classical consensus androgen response element. Increased levels of FSTL1 protein in LAPC-4 cells correlated with higher levels of MAGE-A11 relative to other prostate cancer cells. FSTL1 mRNA levels increased in CRPC and castration-recurrent CWR22 xenografts in association with predominantly nuclear FSTL1. Increased nuclear localization of FSTL1 in prostate cancer was suggested by predominantly cytoplasmic FSTL1 in benign prostate epithelial cells and predominantly nuclear FSTL1 in epithelial cells in CRPC tissue and the castration-recurrent CWR22 xenograft. AR expression studies showed nuclear colocalization of AR and endogenous FSTL1 in response to androgen."
According to the news editors, the research concluded: "AR and MAGE-A11 cooperate in the up-regulation of FSTL1 to promote growth and progression of CRPC."
For more information on this research see: Up-Regulation of Follistatin-Like 1 By the Androgen Receptor and Melanoma Antigen-A11 in Prostate Cancer. Prostate, 2017;77(5):505-516. Prostate can be contacted at: Wiley, 111 River St, Hoboken 07030-5774, NJ, USA. (Wiley-Blackwell - www.wiley.com/; Prostate - onlinelibrary.wiley.com/journal/10.1002/(ISSN)1097-0045)
The news editors report that additional information may be obtained by contacting E.M. Wilson, University of North Carolina, Dept. of Biochem & Biophys, Chapel Hill, NC, United States. Additional authors for this research include A.B. Parris, G. Grossman, J.L. Mohler, Z. Wang and E.M. Wilson (see also Oncology - Prostate Cancer).
Keywords for this news article include: Chapel Hill, North Carolina, United States, North and Central America, Transcription Factors, DNA-Binding Proteins, Prostatic Neoplasms, Androgen Receptors, Steroid Receptors, Xenotransplantion, Carrier Proteins, Prostate Cancer, Biotechnology, Retroviridae, Follistatin, RNA Viruses, Xenografts, Lentivirus, Oncology, Genetics, Melanoma, University of North Carolina.
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