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Oncogenesis v.7 no.5, 2018년, pp.43 - 43   SCIE
본 등재정보는 저널의 등재정보를 참고하여 보여주는 베타서비스로 정확한 논문의 등재여부는 등재기관에 확인하시기 바랍니다.

AIRE promotes androgen-independent prostate cancer by directly regulating IL-6 and modulating tumor microenvironment

Kalra, Rashi    (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India   ); Bhagyaraj, Ella    (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India   ); Tiwari, Drishti    (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India   ); Nanduri, Ravikanth    (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India   ); Chacko, Anuja P.    (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India   ); Jain, Monika    (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India   ); Mahajan, Sahil    (Department of Molecular Biology, Council of Scientific and Industrial  ); Khatri, Neeraj   Gupta, Pawan  
  • 초록  

    Early stage prostate cancers are dependent on androgens for their growth and survival and androgen withdrawal causes them to regress. Progressive prostate cancers eventually acquire androgen independence rendering anti-androgen therapy ineffective. However, the factors leading to this have not been adequately addressed. This study shows that AIRE finds differential expression in androgen-dependent and -independent prostate cancer cells. AIRE expression is more in androgen-independent cells due to its regulation by transcription factor Elk-1. These enhanced levels of AIRE modulate the prostate tumor microenvironment by transcriptionally activating a malignancy gene IL-6 in androgen-independent cells. Additionally, AIRE prevents the cancer cells from anticancer drug-induced death and enhances their invasiveness. Moreover, AIRE by modulating the cytokine milieu skews the tumor-associated macrophage polarization towards M2 phenotype with increased CD206 and CD163 expression. Subcutaneous mouse model of prostate cancer revealed AIRE +/+ mice forming a palpable tumor and presents lymphadenopathy however, only a small benign tumor is observed in AIRE −/− mice and lymph nodes appear normal in size. In conclusion, our findings suggest AIRE as a probable factor in promoting prostate cancer progression.


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