<p>miR-495-3p inhibits the cell proliferation, invasion and migration of osteosarcoma by targeting C1q/TNF-related protein 3</p>

Abstract

Background: Osteosarcoma (OS) is one of the most common malignant tumors of bone, and microRNAs (miRNAs/miRs) serve critical roles in the progression of human OS. The aim of the present study was to investigate the role of miR-495-3p in OS. Methods: The expression of miR-495-3p in OS tissues and adjacent tissues from 30 patients was measured by reverse transcription-quantitative PCR (RT-qPCR). Human OS cell lines (U-2 OS, MG-63 and Saos-2 cells) and normal osteoplastic cells (hFoB 1.19 cells) were employed to perform the further analysis. The cell proliferation ability of MG-63 cells was measured by Cell Counting Kit-8 assay and colony formation assay. In addition, cell invasion and migration were evaluated by Transwell and scratch wound healing assays, respectively. Flow cytometry was applied to assess cell apoptosis and the cell cycle. Moreover, RT-qPCR and Western blotting were performed to measure mRNA and protein expression. A luciferase reporter assay was used to verify the target gene of miR-495-3p. Furthermore, a xenograft OS model was made to evaluate the effect of miR-495-3p in vivo. Results: The results revealed that miR-495-3p was downregulated in the OS tissues and GBM cell lines. Additionally, miR-495-3p overexpression suppressed the proliferation, migration and invasion of MG-63 cells. Simultaneously, cell apoptosis was promoted, accompanied by cell cycle arrest, after transfecting with miR-495-3p mimics. In addition, the expression levels of cell apoptosis-related proteins were increased, whereas proteins of the cell cycle were decreased. Importantly, C1q/TNF-related protein 3 (CTRP3) was confirmed as a direct target of miR-495-3p. A xenograft tumor model was employed to verify the effects of miR-495-3p on OS. Conclusion: On the basis of these results, we conclude that miR-495-3p overexpression inhibited cell proliferation, migration and invasion by downregulating CTRP3. Therefore, miR-495-3p may act as a tumor suppressor and an underlying target for OS treatment.

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

“…It has been reported that miR-495-3p participates in the regulation of tumor cell bioactivity. For example, miR-495-3p regulates osteosarcoma cell apoptosis by targeting C1q/TNF-related protein 3 (32). To investigate the roles of miR-495-3p in CRC cell proliferation, miR-495-3p was effectively overexpressed in the SW480 and LoVo cells (P<0.01; Fig.…”

Long non-coding RNA NORAD exhaustion represses prostate cancer progression through inhibiting TRIP13 expression via competitively binding to miR-495-3p

“…MiR-495-3p was revealed to exert a suppressive role in a range of cancers. One report revealed that miR-495-3p upregulation could repress cell migration, invasion, and proliferation in osteosarcoma cells [18]. Wang et al reported that lncRNA LUCAT1 depletion increased miR-495-3p expression in clear cell renal cell cancer cells, which could suppress cancer cell [35].…”

“…In recent years, miRNAs are revealed to be abnormally expressed in tumors and have attracted widespread attention [15]. MicroRNA-495-3p (miR-495-3p) was showed to be downregulated in a series of tumors, such as colon cancer [16], melanoma [17], and osteosarcoma [18]. MiR-495-3p served as a suppressor in gastric carcinogenesis via modulating multiple epigenetic modifiers [19].…”

miR‐495 and miR‐5688 are down‐regulated in non‐small cell lung cancer under hypoxia to maintain interleukin‐11 expression

“…Because of the relative stability of miRNA expression, some studies have used miRNAs as biomarkers [28]. Recent studies have found that miR-495 was involved in the tumorigenesis and progression of various cancers, including lung cancer [11], nasopharyngeal carcinoma [29], osteosarcoma [30], and melanoma [31]. All of these studies have identified miR-495 as a tumor suppressor.…”