lncRNA DGCR5 Up-Regulates TGF-[beta]1, Increases Cancer Cell Sternness and Predicts Survival of Prostate Cancer Patients

Background: Long non-coding RNA (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) plays different roles in different types of human cancer, but its role in prostate cancer (PC) has not been reported. Methods: DGCR5 and TGF-[beta]1 expression in paired tumor and adjacent healthy tissues from...

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Veröffentlicht in:Cancer management and research 2019-12, p.10657
Hauptverfasser: Li, Bin, Guo, Zhirui, Liang, Quan, Zhou, Huiling, Luo, Yanping, He, Shuyun, Lin, Zhe
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Sprache:eng
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Zusammenfassung:Background: Long non-coding RNA (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) plays different roles in different types of human cancer, but its role in prostate cancer (PC) has not been reported. Methods: DGCR5 and TGF-[beta]1 expression in paired tumor and adjacent healthy tissues from 64 PC patients was analyzed by performing RT-qPCR. A 5-year follow-up study was performed to analyze the prognostic value of DGCR5 for PC. The interaction between DGCR5 and TGF-[beta]1 was analyzed by overexpression experiments. Cell stemness was analyzed by cell stemness assay. Results: In our study, we found that DGCR5 was down-regulated in tumor tissues than in adjacent healthy tissues of PC patients, but TGF-[beta]1 was up-regulated in the tumor tissues. DGCR5 expression was not affected by clinical stages, but low DGCR5 level in the tumor was correlated with poor survival. DGCR5 and TGF-[beta]1 were inversely correlated in tumor tissues but not in adjacent healthy tissues. DGCR5 over-expression resulted in down-regulation of TGF-[beta]1, while TGF-[beta]1 treatment did not significantly affect DGCR5 expression. DGCR5 over-expression led to decreased stemness of PC cells, but TGF-[beta]1 treatment played a reverse role and attenuated the effects of DGCR5 over-expression. DGCR5 may decrease the stemness of PC cells by down-regulating TGF-[beta]1. Keywords: prostate cancer, lncRNA DGCR5, TGF-[beta]1, stemness
ISSN:1179-1322
1179-1322
DOI:10.2147/CMAR.S231112