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Abstract
RNF2, also known as RING1b or RING2, is identified as the catalytic subunit of polycomb repressive complex 1 (PRC1), which mediates the mono-ubiquitination of histone H2A. RNF2 has been proved to have oncogenic function in many kinds of cancers, but the function of RNF2 in prostate cancer (PCa) has not been evaluated. Here we show that PCa tissues showed higher RNF2 expression than the benign prostatic hyperplasia (BPH) tissues. Knockdown of RNF2 in PCa cells resulted in cell cycle arrest, increased apoptosis and inhibited cell proliferation, and the growth of RNF2 knockdown PCa xenografts were obviously inhibited in nude mice. Gene microarray analysis was performed and tumor suppressor gene TXNIP was found to be significantly increased in RNF2 knockdown cells. Simultaneously knockdown of RNF2 and TXNIP can partially rescue the arrested cell cycle, increased apoptosis and inhibited cell proliferation in RNF2 single knockdown cells. Furthermore, ChIP assay result showed that RNF2 enriched at the TXNIP promoter, and the enrichment of RNF2 and ubiquitination of H2A in TXNIP promoter was obviously inhibited in RNF2 knockdown cells. In conclusion, our results demonstrate that RNF2 functions as an oncogene in PCa and RNF2 may regulate the progression of PCa through the inhibition of TXNIP.
Highlights
Prostate cancer (PCa) is the most common malignancy and the second leading cause of cancer death in men, which causes 913,000 new cases and over 261,000 deaths worldwide each year [1]
We showed that RNF2 is highly expressed in prostate cancer (PCa) tissues than the benign prostatic hyperplasia (BPH) tissues, and knockdown of RNF2 in PCa cells resulted in cell cycle arrest, increased apoptosis and inhibited cell proliferation
These results indicate that PCa tissues have higher RNF2 expression than BPH tissues, and the RNF2 level is positively correlated with tumor grade, indicating that RNF2 may have an oncogenic function in PCa
Summary
Prostate cancer (PCa) is the most common malignancy and the second leading cause of cancer death in men, which causes 913,000 new cases and over 261,000 deaths worldwide each year [1]. Stage PCa can be cured by surgery or radiation, but advanced PCa is not curable. Systemic androgen ablation is the mainstay of therapy for disseminated PCa, which aims to suppress the androgen receptor (AR) mediated survival signaling. Inhibition of androgen function, together with or without cytotoxic chemotherapy, is only palliative, but not curative. Until now there have no validated molecular targets for PCa. the identification of novel therapeutic targets and the development of new strategies for the treatment of PCa are urgently required
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