@article{open2184,
          volume = {7},
          number = {5},
           month = {May},
          author = {Rashi Kalra and Ella Bhagyaraj and Drishti Tiwari and Ravikanth Nanduri and Anuja P Chacko and Monika Jain and Sahil Mahajan and Neeraj Khatri and Pawan Gupta},
            note = {Open Access},
           title = {AIRE promotes androgen-independent prostate cancer by directly regulating IL-6 and modulating tumor microenvironment.},
       publisher = {Springer Nature},
            year = {2018},
         journal = {Oncogenesis},
           pages = {1--15},
             url = {http://crdd.osdd.net/open/2184/},
        abstract = {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.}
}