Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 20, Pages -Publisher
MDPI
DOI: 10.3390/ijms232012219
Keywords
prostate cancer (PCa); androgen-responsive lncRNA; 1; c-Myc
Funding
- Shanghai Science and Technology Development Foundation [20ZR1404500]
- Science and Technology Research Program of Shanghai [19DZ2282100]
- Open Research Funds of the State Key Laboratory of Genetic Engineering, Fudan University [SKLGE-1901]
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Long noncoding RNA RP11-1023L17.1 is highly expressed in prostate cancer and acts as an oncogene by enhancing c-Myc protein stability through repression of FBXO32 mRNA expression.
Long noncoding RNAs (lncRNAs) have been found as novel participants in the pathophysiology of prostate cancer (PCa), which is predominantly regulated by androgen and its receptor. The biological function of androgen-responsive lncRNAs remains poorly understood. Here, we identified that lncRNA RP11-1023L17.1, which is highly expressed in PCa. RP11-1023L17.1 expression, can be directly repressed by the androgen receptor in PCa cells. RP11-1023L17.1 depletion inhibited the proliferation, migration, and cell cycle progression, and promoted the apoptosis of PCa cells, indicating that RP11-1023L17.1 acts as an oncogene in PCa cells. Microarray results revealed that RP11-1023L17.1 depletion downregulated the c-Myc transcription signature in PCa cells. RP11-1023L17.1 depletion-induced cellular phenotypes can be overcome by ectopically overexpressed c-Myc. Mechanistically, RP11-1023L17.1 represses FBXO32 mRNA expression, thereby enhancing c-Myc protein stability by blocking FBXO32-mediated c-Myc degradation. Our findings reveal the previously unrecognized roles of RP11-1023L17.1 in c-Myc-dependent PCa tumorigenesis.
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