TY  - JOUR
N1  - Open Access
ID  - open2184
UR  - https://www.nature.com/articles/s41389-018-0053-7
IS  - 5
A1  - Kalra, Rashi
A1  - Bhagyaraj, Ella
A1  - Tiwari, Drishti
A1  - Nanduri, Ravikanth
A1  - Chacko, Anuja P
A1  - Jain, Monika
A1  - Mahajan, Sahil
A1  - Khatri, Neeraj
A1  - Gupta, Pawan
Y1  - 2018/05/25/
N2  - 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.
PB  - Springer Nature
JF  - Oncogenesis
VL  - 7
SN  - 2157-9024
TI  - AIRE promotes androgen-independent prostate cancer by directly regulating IL-6 and modulating tumor microenvironment.
SP  - 1
EP  - 15
ER  -