The Circular RNA Circ_0085494 Regulates Prostate Cancer Progression Through NRBP1/miR-497-5p Axis.

Aberrant expression of circular RNA (circRNA) is closely linked to the progression of various human cancers, including prostate cancer (PCa). In this research, we aimed to investigate the biological role of and mechanisms of circ_0085494 in PCa. The quantitative real-time polymerase chain reaction (qRT-PCR) assay was used to detect circ_0085494, miR-497-5p, and nuclear receptor binding protein 1 (NRBP1) mRNA expression in PCa tissues and cell lines. Subsequently, colony formation, cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), and transwell assays were performed to evaluate PCa cell proliferation, migration, and invasion. Western blot assay was applied for assessing the protein levels. Dual-luciferase reporter and RNA pull-down assays were implemented for verifying the association between miR-497-5p and circ_0085494 or NRBP1. The role of circ_0085494 in vivo was measured by establishing a mice xenograft model. Circ_0085494 was highly expressed in PCa tissues and cells, and its absence suppressed PCa cell proliferation, migration, and invasion. Circ_0085494 impacts NRBP1 content by adsorbing miR-497-5p. Meanwhile, the repression of circ_0085494 absence on tumor growth in vivo was validated. Our finding revealed that circ_0085494 downregulation might repress PCa tumor progression through in part regulating the miR-497-5p/NRBP1 pathway.

Long non-coding RNA SNHG6 regulates the sensitivity of prostate cancer cells to paclitaxel by sponging miR-186.

BACKGROUND: Chemo-resistance is one of the main obstacles in the treatment of prostate cancer (PCa). Long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) is involved in the chemo-resistance of various tumors. We aim to survey the role and underlying molecular mechanism of SNHG6 in PCa resistance to paclitaxel (PTX). METHODS: The expression of SNHG6 and miR-186 was detected using quantitative real time polymerase chain reaction (qRT-PCR). The proliferation, migration, invasion, and apoptosis of PTX-resistant PCa cells were determined via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), transwell assay, or flow cytometry assay. Protein levels of CyclinD1, matrix metalloproteinase 9 (MMP9), Vimentin, E-cadherin, Cleaved-caspase-3 (Cleaved-casp-3) Cleaved-caspase-9 (Cleaved-casp-9), Multidrug Resistance associated Protein 1 (MRP1), and multidrug resistance-1 (MDR1) were assessed by western blot analysis. The relationship between SNHG6 and miR-186 were confirmed by dual-luciferase reporter assay. The role of SNHG6 in vivo was confirmed by xenograft tumor model. RESULTS: SNHG6 expression was increased and miR-186 expression was reduced in drug-resistant PCa tissues and cells. SNHG6 knockdown elevated PTX-resistant PCa cells sensitivity to PTX in vitro and in vivo, and repressed proliferation, migration, and invasion of PTX-resistant PCa cells in vitro. Importantly, SNHG6 acted as a sponge of miR-186. Furthermore, miR-186 downregulation reversed SNHG6 silencing-mediated cell sensitivity to PTX, proliferation, migration, and invasion in PTX-resistant PCa cells. CONCLUSIONS: SNHG6 knockdown elevated the sensitivity of PTX-resistant PCa cells to PTX by sponging miR-186, indicating that SNHG6 might be a therapeutic target for PCa.