Abstract
Increasing evidence demonstrated that noncoding RNAs (lncRNA, miRNA) play important roles in the cancer development. LncRNA NEAT1 functions as an oncogene in many cancers. However, the roles of NEAT1 in prostate cancer (PCa) remain largely unknown. In the present study, we aim to explore the molecular mechanism of NEAT1 in the development of PCa. We detected the expression levels of NEAT1 in a total of 16 benign prostatic hyperplasia tissues (BPH), 30 matched adjacent healthy control (HC) tissues and 30 PCa tissues, as well as PCa cell lines PC-3, DU-145, LNCaP and normal prostate epithelial cell line RWPE-1. The results showed that NEAT1 was significantly up-regulated in PCa tissues and PCa cell lines. Knockdown of NEAT1 can largely inhibit DU-145 and PC-3 cell growth and invasion. Bioinformatics analysis predicted NEAT1 has the binding site of miR-98-5p which can bind to the 3′UTR of HMGA2. And the expression level of NEAT1 has a positive correlation with HMAG2, while negative correlation with miR-98-5p in PCa cells. In addition, luciference assay and RNA immunoprecipitation (RIP) assay confirmed that NEAT1 can function as a competing endogenous RNA (ceRNA) by sponging miR-98-5p to active HMGA2. Moreover, silencing of HMGA2 can decrease the proliferation ability of PCa cells. Taken together, NEAT1/miR-98-5p/HMGA2 pathway is involved in the development and progression of PCa. NEAT1 could be recommended as a prognostic biomarker and inhibition of NEAT1 expression may be a promising strategy for PCa therapy.
Highlights
Prostate cancer (PCa) is the most common malignancy and the second leading cause of cancer death among men worldwide [1]
NEAT1 level exhibits no obvious difference in benign prostatic hyperplasia tissues (BPH) and healthy control (HC) tissues (P>0.05, Figure 1A), it is clearly showed that the expression level of NEAT1 is significantly up-regulated in PCa tissues, compared with BPH (P
The overexpression of NEAT1 in PCa is validated in cell lines, as shown that NEAT1 is up-regulated in DU145, PC3 and LNCaP PCa cell lines compared with normal prostate epithelial cell line RWPE- 1 (Figure 1C)
Summary
Prostate cancer (PCa) is the most common malignancy and the second leading cause of cancer death among men worldwide [1]. The occurrence and development of PCa is a multi-step process involving in the deregulation of many oncogenes and tumor suppressor genes. It is urgent to explore the molecular mechanisms underlying PCa and develop promising diagnostic and prognostic biomarkers for cancer diagnosis and treatment. LncRNAs, a class of non-coding RNAs with the length ranging from 200 nucleotides to almost 100 kilobases, play important roles in cancer progression and development [4]. Accumulating evidences showed that lncRNAs are involved in several cell biological processes including cell growth, differentiation, apoptosis, angiogenesis, migration, invasion, metastasis and cell-cycle progression [5,6]. Recent studies demonstrated that lncRNAs function as miRNA sponges and exert their oncogenic or tumor suppressive effect [7], which suggesting the pivotal roles of lncRNAs in the development and progression of PCa
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