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MicroRNA-193b regulates human ovarian cancer cell growth via targeting STMN1.

ABSTRACT: Ovarian cancer is the eighth most common malignancy among women worldwide. Ovarian cancer exhibits no obvious symptoms in the early stage of tumorigenesis and currently, no effective methods for the early detection and treatment of ovarian cancer have been established. Therefore, the identification of novel targets is critical to the early diagnosis and clinical treatment of ovarian cancer. microRNAs (miRs) are small non-coding RNAs, which serve an important biological role in a number of physiological processes and in oncogenesis. Previous studies have reported that miRNA-193b is dysregulated in a variety of types of human cancer. However, the roles of miRNA-193b in human ovarian cancer has not been determined. The present study investigated the roles of miRNA-193b in human ovarian cancer cells. Reverse transcription-quantitative PCR results indicated that the expression of miRNA-193b in ovarian cancer cells was significantly down-regulated compared with non-malignant cells. Cell counting kit-8 results indicated that the up-regulation of miRNA-193b inhibited ovarian cancer cell proliferation and induced ovarian cancer cell apoptosis. The present study also indicated that stathmin 1 (STMN1) was a direct target of miRNA-193b, and the up-regulation of miRNA-193b significantly decreased the expression of STMN1 in ovarian cancer cells. In conclusion, the results demonstrated that miRNA-193b serves as a tumor suppressor in human ovarian cancer by inhibiting cell proliferation and inducing cell apoptosis. Therefore, the assessment of miRNA-193b may provide insight into a novel diagnostic biomarker and potential therapeutic target for patients with ovarian cancer.

SUBMITTER: Li H

PROVIDER: S-EPMC7444320 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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MicroRNA-193b regulates human ovarian cancer cell growth via targeting STMN1.

Li Haiyan H Xu Yuping Y Zhao Danni D

Experimental and therapeutic medicine 20200723 4

Ovarian cancer is the eighth most common malignancy among women worldwide. Ovarian cancer exhibits no obvious symptoms in the early stage of tumorigenesis and currently, no effective methods for the early detection and treatment of ovarian cancer have been established. Therefore, the identification of novel targets is critical to the early diagnosis and clinical treatment of ovarian cancer. microRNAs (miRs) are small non-coding RNAs, which serve an important biological role in a number of physio ...[more]

PMID: 32855702

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Project description:Histone deacetylase 3 (HDAC3) plays a pivotal role in the repression of cartilage-specific gene expression in human chondrocytes. The aim of this study was to determine whether microRNA-193b-3p (miR-193b-3p) regulates the expression of HDAC3 during chondrogenesis and chondrocyte metabolism. Methods: miR-193b-3p expression was assessed in a human mesenchymal stem cell (hMSC) model of chondrogenesis, in interleukin-1? (IL-1?)-treated primary human chondrocytes (PHCs), and in non-degraded and degraded cartilage. hMSCs and PHCs were transfected with miR-193b-3p or its antisense inhibitor. A direct interaction between miR-193b-3p and its putative binding site in the 3'-untranslated region (3'-UTR) of HDAC3 mRNA was confirmed by performing luciferase reporter assays. Chondrocytes were transfected with miR-193b-3p before performing a chromatin immunoprecipitation assay with an anti-acetylated histone H3 antibody. To investigate miR-193b-3p-transfected PHCs in vivo, they were seeded in tricalcium phosphate-collagen-hyaluronate (TCP-COL-HA) scaffolds, which were then implanted in nude mice. In addition, plasma exosomal miR-193b-3p in samples from normal controls and patients with osteoarthritis (OA) were measured. Results: miR-193b-3p expression was elevated in chondrogenic and hypertrophic hMSCs, while expression was significantly reduced in degraded cartilage compared to non-degraded cartilage. In addition, miR-193b-3p suppressed the activity of reporter constructs containing the 3'-UTR of HDAC3, inhibited HDAC3 expression, and promoted histone H3 acetylation in the COL2A1, AGGRECAN, COMP, and SOX9 promoters. Treatment with the HDAC inhibitor trichostatin A (TSA) increased cartilage-specific gene expression and enhanced hMSCs chondrogenesis. TSA also increased AGGRECAN expression and decreased MMP13 expression in IL-1?-treated PHCs. Further, 8 weeks after implanting PHC-seeded TCP-COL-HA scaffolds subcutaneously in nude mice, we found that miR-193b overexpression strongly enhanced in vivo cartilage formation compared to that found under control conditions. We also found that patients with OA had lower plasma exosomal miR-193b levels than control subjects. Conclusions: These findings indicate that miR-193b-3p directly targets HDAC3, promotes H3 acetylation, and regulates hMSC chondrogenesis and metabolism in PHCs.

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MicroRNA-193b regulates human ovarian cancer cell growth via targeting STMN1.

Publications

MicroRNA-193b regulates human ovarian cancer cell growth via targeting STMN1.

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