Abstract
Background Prostate cancer (PCa) is one of the most common malignancies in men. Increasing evidence has demonstrated that dysregulation of long noncoding RNAs (lncRNAs) is closely related to carcinogenesis and cancer progression. lncRNA NEAT1 has recently been identified as a carcinogenic regulator of multiple cancers; however, the role of NEAT1 on PCa is still poorly understood. Methods Kaplan–Meier was conducted to determine the overall survival rate in PCa patients with aberrant NEAT1 levels. qRT-PCR analysis was performed to detect expressions of NEAT1 and miR-766-5p in tissues and cells. In addition, CCK-8, colony formation, flow cytometry analysis, wound healing, and transwell assay were conducted to determine cell proliferation, cell arrest, apoptosis, migration, and invasion. The western blot assay was utilized to determine E2F3 and cell growth-related proteins. The relationship between NEAT1 and miR-766-5p or miR-766-5p and E2F3 was verified by correlation analysis and dual-luciferase reporter assay. Results Here, we find that NEAT1 is overexpressed in PCa tissues and cell lines. Besides, silencing of NEAT1 inhibits cell proliferation, invasion, and migration and promotes cell apoptosis and cell cycle arrest. Further mechanistic studies find that NEAT1 sponges miR-766-5p, and miRNA-766-5p is negatively correlated with the expression of NEAT1. In addition, the functional experiment shows that upregulation of miRNA-766-5p inhibits PCa proliferation, migration, and invasion. Furthermore, E2F transcription factor 3 (E2F3) is testified to be the downstream target gene of miRNA-766-5p. Finally, the rescue experiment revealed that miRNA-766-5p inhibition largely restores NEAT1 downregulation-mediated function on PCa progression, while E2F3 knockdown partly removes the effects of miRNA-766-5p inhibitor. Conclusions In conclusion, NEAT1 facilitates PCa progression by targeting the miRNA-766-5p/E2F3 axis.
Highlights
As one of the most common malignant tumors in the male urinary system, prostate cancer (PCa) is a malignant tumor occurring in the prostatic epithelium [1]
Growing evidence has indicated that long noncoding RNAs (lncRNAs) are involved in various pathologic processes of cancer by regulating gene expressions at epigenetic, transcriptional, and post-transcriptional levels [15]
For Prostate cancer (PCa) oncogenesis, abundant lncRNAs with carcinogenic or anticancer roles have been proved to be involved in this process [16, 17]
Summary
As one of the most common malignant tumors in the male urinary system, prostate cancer (PCa) is a malignant tumor occurring in the prostatic epithelium [1]. According to the previous studies, lncRNAs regulate miRNAs expression in competitive endogenous RNAs (ceRNAs) form [11]. LncRNA SNHG14 promotes the tumorigenesis of PCa via targeting miR-5590-3p to regulate YY1 expression [12]. For another example, knockdown of lncRNA LOXL1-AS1 inhibits the occurrence and development of PCa via the miR-541-3p/CCND1 axis [13]. The functional experiment shows that upregulation of miRNA-766-5p inhibits PCa proliferation, migration, and invasion. The rescue experiment revealed that miRNA-766-5p inhibition largely restores NEAT1 downregulation-mediated function on PCa progression, while E2F3 knockdown partly removes the effects of miRNA-766-5p inhibitor. NEAT1 facilitates PCa progression by targeting the miRNA-766-5p/E2F3 axis
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