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miR‐2909 regulates ISGylation system via STAT1 signalling through negative regulation of SOCS3 in prostate cancer
Author(s) -
Ayub Shiekh Gazalla,
Kaul Deepak
Publication year - 2017
Publication title -
andrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.947
H-Index - 43
eISSN - 2047-2927
pISSN - 2047-2919
DOI - 10.1111/andr.12374
Subject(s) - prostate cancer , cancer research , stat1 , stat , biology , smad , carcinogenesis , cancer , interferon , immune system , cytokine , stat3 , signal transduction , immunology , microbiology and biotechnology , genetics
One of the well‐document strategies adopted by tumour cells for progression is to evade immune surveillance mechanisms. An understanding of the tight interaction between immunity and progression of cancer can provide novel treatment options for different malignancies including prostate cancer ( PC a). Here, we have shown that AATF genome encoded miR‐2909, known to play role both in immunity and cancer upregulates various interferon stimulating genes ( ISG s) including ISG ylation system through STAT 1. Our results revealed that miR‐2909 up‐regulates STAT 1 through negative regulation of SOCS 3 and not through up‐regulation of Type 1 interferon ( IFN ) production. It was observed that inhibition of ISG ylation reduced the proliferation potential of PC a cells. Furthermore, androgens were found to negatively regulate ISG ylation in LNC aP cells through androgen receptor signalling independently of miR‐2909. TGF ‐β mediated SMAD 3 signalling was also seen to be suppressed by miR‐2909 through induction of SMAD 7 via enhanced STAT 1 expression. Collectively, these studies suggest that miR‐2909 could play a vital role in prostate carcinogenesis through modulation of ISG ylation system and TGF β signalling via STAT 1.