MicroRNA-1180 is associated with growth and apoptosis in prostate cancer via TNF receptor associated factor 1 expression regulation and nuclear factor-κB signaling pathway activation

Zhu,Deyuan; Gao,Wenxi; Zhang,Zhongmin

doi:10.3892/ol.2018.7914

MicroRNA-1180 is associated with growth and apoptosis in prostate cancer via TNF receptor associated factor 1 expression regulation and nuclear factor-κB signaling pathway activation

Authors:
- Deyuan Zhu
- Wenxi Gao
- Zhongmin Zhang
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Affiliations: Department of Urology, Optical Valley School District, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, Hubei 430074, P.R. China
Published online on: January 31, 2018 https://doi.org/10.3892/ol.2018.7914
Pages: 4775-4780
Copyright: © Zhu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

In the present study, the aim was to investigate the role of microRNA-1180 (miR-1180) in the growth and apoptosis of prostate cancer, as well as to identify its direct targets. Initially, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to examine the expression of miR‑1180 in the prostate cancer tissues and adjacent normal prostate tissues of 30 patients, as well as in DU145 and RWPE‑1 cells. Next, DU145 cells were transfected with miR‑1180 mimics, and the expression levels of associated proteins were determined by western blot assay. In addition, the role of miR‑1180 in the proliferation, apoptosis, invasion and migration of DU145 cells was investigated by MTT, flow cytometry, cell invasion and wound healing assays, respectively. A dual‑luciferase reporter assay was also performed to examine whether TNF receptor associated factor 1 (TRAF1) and B‑cell lymphoma‑2‑associated athanogene 2 (BAG2) are direct targets of miR‑1180. It was observed that miR‑1180 expression was significantly decreased in the prostate cancer tissues compared with the normal prostate tissues, and was also inhibited in DU145 cells compared with RWPE‑1 cells. Furthermore, transient overexpression of miR‑1180 inhibited the proliferation, migration and invasion, and promoted the apoptosis of DU145 cells, as well as alleviated expression of associated proteins. The dual‑luciferase reporter assay confirmed that TRAF1 and BAG2 are direct targets of miR‑1180. These results suggested that miR‑1180 contributed to prostate cancer by targeting TRAF1/BAG2 and by nuclear factor‑κB signaling pathway activation.

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