The lncRNA PTTG3P promotes the progression of CRPC via upregulating PTTG1.

BACKGROUND:Overexpression of certain long non-coding RNAs (lncRNAs) promotes the progression of castration-resistant prostate cancer (CRPC). The significance and potential role of the lncRNA designated pituitary tumour-transforming 3, pseudogene in CRPC is unknown. METHODS:We detected expression by qPCR. Upregulated duanyu1547G3P expression was performed to explore the role of duanyu1547G3P in PCa cells resistant to ADT (androgen deprivation therapy). The relationship among mir-146a-3p and were validated by qPCR, western blot and luciferase levels were significantly increased in the androgen-independent PC cell lines, as well as in CRPC tissues compared with those of the androgen-dependent prostate cancer cell line LNCaP and tumour tissues of patients with hormone-naive prostate cancers. Enforced expression of duanyu1547G3P in androgen-deprived LNCaP cells significantly enhanced survival, clonogenicity, and tumorigenicity. Further, duanyu1547G3P acted as a competing endogenous RNA (ceRNA, natural miRNA sponge) to upregulate duanyu1547G1 expression by competing for mir-146a-3p in the progression to CRPC. CONCLUSION:Our findings suggest that duanyu1547G3P promotes the resistance of prostate cancer cells to androgen-deprivation therapy via upregulating duanyu1547G3P may therefore represent a potential target for therapy of CRPC.

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