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Circular RNA SMO sponges miR-338-3p to promote the growth of glioma by enhancing the expression of SMO.

ABSTRACT: Glioma is one of the most common tumors in the brain and complete cure still a challenge. The present research aimed to investigate the molecular mechanism of circular RNA SMO (circSMO742) in glioma, via targeting miR-338-3p and regulating SMO expression. QRT-PCR was utilized to examine the expression profiles of circSMO742 and microRNA-338-3p (miR-338-3p) in glioma. SMO protein in glioma was tested via western blot. RNA pulldown assay and dual luciferase reporter assays were used to explore the targeting correlation between RNAs. MTT assay, transwell assays and flow cytometry were used to investigate cell proliferation, migration and invasion, and apoptosis, respectively. Tumor xenograft was done to ascertain the effect of circSMO742 knocking down on tumor growth. CircSMO742 and SMO were highly expressed in glioma tissues, while miR-338-3p expression was reduced. CircSMO742 together with SMO could promote cells proliferation, migration and invasion while inhibit cells apoptosis, whereas miR-338-3p showed negative impacts on the cell activity. Knocking down of circSMO742 suppressed glioma growing in vivo. CircSMO742 promoted glioma growth by sponging miR-338-3p to regulate SMO expression. Our research revealed a new molecular mechanism of glioma growth and provide a fresh perspective on circRNAs in glioma progression.

SUBMITTER: Xiong Z

PROVIDER: S-EPMC6949074 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Circular RNA SMO sponges miR-338-3p to promote the growth of glioma by enhancing the expression of SMO.

Xiong Zhiyong Z Zhou Chaoyang C Wang Luyang L Zhu Ronglan R Zhong Liangchen L Wan Dengfeng D Wang Qiangping Q

Aging 20191230 24

Glioma is one of the most common tumors in the brain and complete cure still a challenge. The present research aimed to investigate the molecular mechanism of circular RNA SMO (circSMO742) in glioma, via targeting miR-338-3p and regulating SMO expression. QRT-PCR was utilized to examine the expression profiles of circSMO742 and microRNA-338-3p (miR-338-3p) in glioma. SMO protein in glioma was tested via western blot. RNA pulldown assay and dual luciferase reporter assays were used to explore the ...[more]

PMID: 31895689

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Project description:BackgroundCircular RNA microarray analysis showed hsa_circ_0010235 (circ_0010235) was highly upregulated in non-small-cell lung cancer (NSCLC) patients; however, its role in carcinogenesis and development of NSCLC cells was unrevealed. Here, we intended to investigate role and mechanism of circ_0010235 in NSCLC proliferation, migration and invasion.Methods and resultsExpression of circ_0010235, microRNA (miR)-338-3p and kinesin family member 2A (KIF2A) was detected by quantitative real-time PCR, western blotting and immunohistochemistry (IHC). Cell progression was measured by cell-counting kit-8 assay, 5-ethynyl-2-deoxyuridine (EdU) assay, flow cytometry, transwell assay, western blotting, IHC and xenograft experiment. The relationship among circ_0010235, miR-338-3p and KIF2A was determined by dual-luciferase reporter assay, RNA immunoprecipitation and Pearson's correlation analysis. Expression of circ_0010235 was increased in human NSCLC tissues and cells, accompanied with miR-338-3p downregulation and KIF2A upregulation. Essentially, circ_0010235 could sponge miR-338-3p via target binding, and miR-338-3p downstream targeted KIF2A. Functionally, exhaustion of circ_0010235 induced apoptosis rate of NSCLC cells and curbed cell viability, EdU incorporation, migration rate and invasion rate, accompanied with higher E-cadherin and lower N-cadherin expression. Additionally, re-expression of miR-338-3p prompted above similar effects in NSCLC cells in vitro. Contrarily, miR-338-3p blockage partially counteract the effects of circ_0010235 exhaustion; plus, restoration of KIF2A could attenuate miR-338-3p role, as well. Notably, interfering circ_0010235 delayed tumour growth of NSCLC cells by promoting miR-338-3p and E-cadherin expression, and depressing KIF2A, ki-67 and N-cadherin expression.Conclusionscirc_0010235 could be a novel identified oncogenic circRNA in NSCLC, and targeting miR-338-3p/KIF2A axis was one regulatory mechanism underlying circ_0010235.KEY MESSAGECirc_0010235 was an upregulated circRNA in NSCLC patients and cells.Interfering circ_0010235 restrained NSCLC cell proliferation and metastasis in vitro and in vivo.miR-338-3p per se suppressed NSCLC in vitro and its downregulation diminished the tumour-suppressive role of circ_0010235 blockage in NSCLC cells.miR-338-3p could downstream target KIF2A and be sponged by circ_0010235.

Dataset Information

Circular RNA SMO sponges miR-338-3p to promote the growth of glioma by enhancing the expression of SMO.

Publications

Circular RNA SMO sponges miR-338-3p to promote the growth of glioma by enhancing the expression of SMO.

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