Abstract
Prostate cancer is the third most common causes of death from cancer in men. Our previous study demonstrated that lncRNA PVT1 was overexpressed and played an oncogenic role in the progression of prostate cancer. However, the molecular mechanism of modulating the prostate cancer tumorigenesis was still unknown. In this study, we aim to investigate the interaction between PVT1 and miR‐146a in prostate cancer and reveal the potential mechanism in prostate cancer carcinogenesis. The expression level of miR‐146a was assessed by quantitative RT‐PCR. The correlation analysis and methylation status analysis was made to confirm the interaction between PVT1 and miR‐146a. Biological function analysis was performed through gain‐of‐function and loss‐of‐function strategies. Our results showed that miR‐146a was downregulated and negatively correlated with PVT1 level in prostate cancer. PVT1 mediated miR‐146a expression by inducing the methylation of CpG Island in its promoter. miR‐146a overexpression eliminated the effects of PVT1 knockdown on prostate cancer cells. PVT1 regulated prostate cancer cell viability and apoptosis depending on miR‐146a. Our study suggested a regulatory relationship between lncRNA PVT1 and miR‐146a during the process of the prostate cancer tumorigenesis. PVT1 regulated prostate cancer cell viability and apoptosis depending on miR‐146a. It would contribute to the diagnosis, treatment and prognosis of prostate cancer.
Highlights
Prostate cancer is the most common male reproductive tumor the third most common causes of death from cancer in men in the whole world [1,2,3,4]
The antitumor effect of plasmacytoma variant translocation 1 (PVT1) knockdown was counteracted when miR-1 46a was silenced in prostate cancer cells. These results suggested that PVT1 regulated prostate cancer cell viability and apoptosis depending on miR-146a
We confirmed that PVT1 predicted patient prognosis and regulated tumor growth in prostate cancer
Summary
Prostate cancer is the most common male reproductive tumor the third most common causes of death from cancer in men in the whole world [1,2,3,4]. The therapeutic options, such as radical prostatectomy and radiation, could successfully cure the majority of patients, approximately 30–40% of patients will relapse. It is the major cause impairing survival of the patients with prostate cancer [5,6,7]. Recent study found that PVT1 was upregulated in prostate cancer and identified PVT1 as the oncogene to increase the risk of prostate cancer [15, 16]. We demonstrated that PVT1 was overexpressed and played an oncogenic role in the progression of prostate cancer. The target gene of PVT1 and the molecular mechanism of modulating the prostate cancer tumorigenesis were still unknown
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