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Edachery, S. and Patil , P. and Mohan, R. and Mohan , R. and Aradhya, B. and Shetty, J. and Kabekkodu , SP and Santra, MK and Gonchigar, SJ and Shetty, P. (2022) Loss of miR-936 leads to acquisition of androgen- independent metastatic phenotype in prostate cancer. Scientific Report, 12 (1). p. 17070.

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Abstract

Prostate cancer (PCa) progresses from a hormone-sensitive, androgen-dependent to a hormone-refractory, androgen-independent metastatic phenotype. Among the many genes implicated, ANXA2, a calcium-dependent phospholipid binding protein, has been found to have a critical role in the progression of PCa into more invasive metastatic phenotype. However, the molecular mechanisms underlying the absence of ANXA2 in early PCa and its recurrence in advanced stage are yet unknown. Moreover, recent studies have observed the deregulation of microRNAs (miRNAs) are involved in the development and progression of PCa. In this study, we found the down-regulation of miR-936 in metastatic PCa wherein its target ANXA2 was overexpressed. Subsequently, it has been shown that the downregulation of miRNA biogenesis by siRNA treatment in ANXA2-null LNCaP cells could induce the expression of ANXA2, indicating the miRNA mediated regulation of ANXA2 expression. Additionally, we demonstrate that miR-936 regulates ANXA2 expression by direct interaction at coding as well as 3′UTR region of ANXA2 mRNA by luciferase reporter assay. Furthermore, the overexpression of miR-936 suppresses the cell proliferation, cell cycle progression, cell migration, and invasion abilities of metastatic PCa PC-3 cells in vitro and tumor forming ability in vivo. These results indicate that miR-936 have tumor suppressor properties by regulating the over expression of ANXA2 in hormone-independent metastatic PCa. Moreover, our results suggest that this tumor suppressor miR-936 could be developed as a targeted therapeutic molecule for metastatic PCa control and to improve the prognosis in PCa patients.

Item Type: Article
Additional Information: 1 Department of Biochemistry, Kuvempu University, Shankaraghatta, Karnataka, 577451, India. 2 Division of Proteomics and Cancer Biology, Nitte University Center for Science Education and Research, Nitte (Deemed to be University), Mangaluru, Karnataka, 575018, India. 3 Central Research Laboratory, K S Hegde Medical Academy, Nitte (Deemed to be University), Deralakatte, Mangaluru, 575018, India. 4 Department of Surgery, All India Institute of Medical Sciences, Mangalagiri, Andhra Pradesh, 522503, India. 5 HCG-Suchirayu Hospital, Gokul Road, Hubli, 580030, India. 6 Department of Pathology, K S Hegde Medical Academy, Nitte (Deemed to be University), Deralakatte, Mangaluru, 575018, India. 7 School of Life Sciences, Life Science Center, Manipal University, Manipal, 576104, India. 8 National Center for Cell Sciences, Ganesh Kind, Pune, 411007, India. 9 Department of Biochemistry, Kuvempu University, Shankaraghatta, Karnataka, 577451, India. satishlec@gmail.com. 10 Central Research Laboratory, K S Hegde Medical Academy, Nitte (Deemed to be University), Deralakatte, Mangaluru, 575018, India. praveenkumarshetty@nitte.edu.in. 11 Department of Biochemistry, K S Hegde Medical Academy, Nitte (Deemed to be University), Deralakatte, Mangaluru, 575018, India. praveenkumarshetty@nitte.edu.in.
Subjects: Cancer Biology
Depositing User: Mr. Rameshwar Nema
Date Deposited: 11 Jan 2023 10:41
Last Modified: 11 Jan 2023 10:41
URI: http://nccs.sciencecentral.in/id/eprint/1234

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