miR-2909 regulates ISGylation system via STAT1 signalling through negative regulation of SOCS3 in prostate cancer
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Updated: Feb 28, 2026

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR
Published on: May 16, 2012
Shiekh Gazalla Ayub1, Deepak Kaul1
1Department of Experimental Medicine and Biotechnology, Post-Graduate Institute of Medical Sciences and Research, Chandigarh, India.
Abstract:
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 (PCa). Here, we have shown that AATF genome encoded miR-2909, known to play role both in immunity and cancer upregulates various interferon stimulating genes (ISGs) including ISGylation system through STAT1. Our results revealed that miR-2909 up-regulates STAT1 through negative regulation of SOCS3 and not through up-regulation of Type 1 interferon (IFN) production. It was observed that inhibition of ISGylation reduced the proliferation potential of PCa cells. Furthermore, androgens were found to negatively regulate ISGylation in LNCaP cells through androgen receptor signalling independently of miR-2909. TGF-β mediated SMAD3 signalling was also seen to be suppressed by miR-2909 through induction of SMAD7 via enhanced STAT1 expression. Collectively, these studies suggest that miR-2909 could play a vital role in prostate carcinogenesis through modulation of ISGylation system and TGFβ signalling via STAT1.
Insights
MicroRNA-2909 (miR-2909) promotes prostate cancer by upregulating immune-related genes and STAT1. Inhibiting this pathway may offer new prostate cancer (PCa) treatment strategies.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Tumor cells evade immune surveillance for progression.
- Understanding cancer-immunity interactions can yield novel cancer treatments, including for prostate cancer (PCa).
Purpose of the Study:
- To investigate the role of miR-2909 in prostate cancer progression and its interaction with immune and signaling pathways.
- To elucidate the regulatory mechanisms of miR-2909 in PCa.
Main Methods:
- Analysis of miR-2909's effect on interferon-stimulating genes (ISGs) and the ISGylation system via STAT1.
- Investigating miR-2909's regulation of SOCS3 and Type 1 interferon (IFN) production.
- Examining the impact of ISGylation inhibition on PCa cell proliferation.
- Assessing the influence of androgens and TGF-β signaling on ISGylation and miR-2909 activity.
Main Results:
- miR-2909 upregulates ISGs and the ISGylation system through STAT1 by negatively regulating SOCS3, independent of Type 1 IFN production.
- Inhibition of ISGylation significantly reduced PCa cell proliferation.
- Androgens negatively regulate ISGylation in LNCaP cells via androgen receptor signaling, independent of miR-2909.
- miR-2909 suppresses TGF-β mediated SMAD3 signaling by inducing SMAD7 through enhanced STAT1 expression.
Conclusions:
- miR-2909 plays a significant role in prostate carcinogenesis.
- Modulation of the ISGylation system and TGF-β signaling via STAT1 by miR-2909 are key mechanisms in PCa.
- Targeting miR-2909 or its downstream pathways presents a potential therapeutic strategy for prostate cancer.
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