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MicroRNA-136-3p inhibits glioma tumorigenesis in vitro and in vivo by targeting KLF7.

ABSTRACT: BACKGROUND:Malignant brain tumors have been a serious threat to human health worldwide. This study aims to investigate the role of miR-136-3p in glioma development. METHODS:Hematoxylin-eosin staining (H&E) staining was used to determine the pathologic alterations of glioma tissues. Quantitative real-time PCR (qRT-PCR) analysis and GEO2R analysis was performed to examine the expression of miRNAs and genes. Western blot was applied to detect the protein expression. Cell counting kit-8 (CCK-8) and colony formation were used to analyze the glioma cell growth. Trans-well assay was used to determine the cell migration. Annexin V-FITC/PI staining was conducted to determine the cell apoptosis of transfected glioma cells. The dual-luciferase reporter assay was carried out to confirm the binding sites of miR-136-3p on 3' untranslated regions (3' UTR) of Kruppel-like factor 7 (KLF7). Tumor-bearing experiment in nude mice was performed to comprehensively investigate the role of miR-136-3p/KLF7 axis in gliomas. RESULTS:Firstly, the results showed that miR-136-3p was decreased in glioma tissues compared with adjacent tissues. Overexpression of miR-136-3p significantly inhibited cell growth of LN-229 and U251 by decreasing expression of Cyclin A1 and PCNA (proliferating cell nuclear antigen), and it suppressed glioma cell migration by downregulating N-cadherin and elevating E-cadherin levels, and it also promotes glioma cell apoptosis by promoting Bcl2-associated X (Bax) expression but suppressing Bcl-2 expression. Furthermore, we observed that KLF7 was a direct target of miR-136-3p, and KLF7 was negatively regulated by miR-136-3p in glioma cells. Finally, overexpression of KLF7 partly blocked miR-136-3p-induced inhibition of tumor growth in vitro and in vivo. CONCLUSIONS:Targeting miR-136-3p/KLF7 axis might be a novel manner to counter against gliomas.

SUBMITTER: Xu Y

PROVIDER: S-EPMC7367243 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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MicroRNA-136-3p inhibits glioma tumorigenesis in vitro and in vivo by targeting KLF7.

Xu Yanwu Y

World journal of surgical oncology 20200716 1

<h4>Background</h4>Malignant brain tumors have been a serious threat to human health worldwide. This study aims to investigate the role of miR-136-3p in glioma development.<h4>Methods</h4>Hematoxylin-eosin staining (H&E) staining was used to determine the pathologic alterations of glioma tissues. Quantitative real-time PCR (qRT-PCR) analysis and GEO2R analysis was performed to examine the expression of miRNAs and genes. Western blot was applied to detect the protein expression. Cell counting kit ...[more]

PMID: 32677950

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Project description:BackgroundEmerging evidence suggests that microRNAs (miRs) are associated with the progression of osteoarthritis (OA). In this study, the role of exosomal miR-136-5p derived from mesenchymal stem cells (MSCs) in OA progression is investigated and the potential therapeutic mechanism explored.MethodsBone marrow mesenchymal stem cells (BMMSCs) and their exosomes were isolated from patients and identified. The endocytosis of chondrocytes and the effects of exosome miR-136-5p on cartilage degradation were observed and examined by immunofluorescence and cartilage staining. Then, the targeting relationship between miR-136-5p and E74-like factor 3 (ELF3) was analyzed by dual-luciferase report assay. Based on gain- or loss-of-function experiments, the effects of exosomes and exosomal miR-136-5p on chondrocyte migration were examined by EdU and Transwell assay. Finally, a mouse model of post-traumatic OA was developed to evaluate effects of miR-136-5p on chondrocyte degeneration in vivo.ResultsIn the clinical samples of traumatic OA cartilage tissues, we detected increased ELF3 expression, and reduced miR-136-5p expression was determined. The BMMSC-derived exosomes showed an enriched level of miR-136-5p, which could be internalized by chondrocytes. The migration of chondrocyte was promoted by miR-136-5p, while collagen II, aggrecan, and SOX9 expression was increased and MMP-13 expression was reduced. miR-136-5p was verified to target ELF3 and could downregulate its expression. Moreover, the expression of ELF3 was reduced in chondrocytes after internalization of exosomes. In the mouse model of post-traumatic OA, exosomal miR-136-5p was found to reduce the degeneration of cartilage extracellular matrix.ConclusionThese data provide evidence that BMMSC-derived exosomal miR-136-5p could promote chondrocyte migration in vitro and inhibit cartilage degeneration in vivo, thereby inhibiting OA pathology, which highlighted the transfer of exosomal miR-136-5p as a promising therapeutic strategy for patients with OA.

Dataset Information

MicroRNA-136-3p inhibits glioma tumorigenesis in vitro and in vivo by targeting KLF7.

Publications

MicroRNA-136-3p inhibits glioma tumorigenesis in vitro and in vivo by targeting KLF7.

Similar Datasets

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