Dataset Information

MicroRNA-183-5p Inhibits Aggressiveness of Cervical Cancer Cells by Targeting Integrin Subunit Beta 1 (ITGB1).

ABSTRACT: BACKGROUND Accumulating studies demonstrate that microRNAs play crucial roles in multiple processes of cancer progression. Lower levels of miR-183 have been observed in diverse types of tumors but the mechanism and precise function of miR-183-5p in cervical cancer have largely not been investigated. MATERIAL AND METHODS The level of miR-183-5p in different cervical cancer cell lines and clinical tissues was detected qRT-PCR assays. Transwell and wound-healing migration assays were conducted to assess the functional roles of miR-183-5p in over-expressing cervical cancer cells in vitro. Rescue assays were carried out to confirm the contribution of integrin subunit Beta 1 (ITGB1) to the aggressiveness of cancer cells regulated by miR-183-5p. RESULTS miR-183-5p was reduced in clinical tissues of cervical cancer and cell lines when compared to the normal subjects and normal cervical epithelial cell line, respectively. In addition, over-expression of miR-183-5p markedly inhibited migration and invasion in cervical cancer cells, and increased aggressiveness was observed in miR-183-5p inhibitor transfected cells. Furthermore, the luciferase reporter assays revealed that ITGB1 was the gene directly regulated by miR-183-5p. Notably, a negative association between the ITGB1 and miR-183-5p was found, and the gene expressions of ITGB1 was mediated by miR-183-5p in cervical cancer cells. CONCLUSIONS miR-183-5p serves as a latent anti-oncogene by targeting the metastasis-promoter gene, ITGB1.

SUBMITTER: Zhang W

PROVIDER: S-EPMC6190727 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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MicroRNA-183-5p Inhibits Aggressiveness of Cervical Cancer Cells by Targeting Integrin Subunit Beta 1 (ITGB1).

Zhang Wei W Zhang Mingkai M Liu Lantao L Jin Dan D Wang Pengyu P Hu Jing J

Medical science monitor : international medical journal of experimental and clinical research 20181007

BACKGROUND Accumulating studies demonstrate that microRNAs play crucial roles in multiple processes of cancer progression. Lower levels of miR-183 have been observed in diverse types of tumors but the mechanism and precise function of miR-183-5p in cervical cancer have largely not been investigated. MATERIAL AND METHODS The level of miR-183-5p in different cervical cancer cell lines and clinical tissues was detected qRT-PCR assays. Transwell and wound-healing migration assays were conducted to a ...[more]

PMID: 30293085

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Project description:Glioblastoma (GBM) is the most common malignant primary brain tumor, accounting for ~57% of all gliomas and 48% of all malignant primary central nervous system tumors in the United States. Abnormal expression of the replication factor C subunit 2 (RFC2) gene and microRNA (miR)-744-5p is associated with tumorigenic characteristics, including cellular proliferation, migration and invasiveness. However, the mechanism underlying the interaction between miR-744-5p and RFC2 in GBM remains unknown. Reverse transcription-quantitative (RT-q) PCR analysis of RFC2 and miR-744-5p was performed using GBM tumor tissues and cells, and the association between miR-744-5p and RFC2 was determined by dual-luciferase reporter assay. Cell Counting Kit 8, 5-bromo-2-deoxyuridine (BrdU), wound-healing and cellular adhesion assays, as well as the detection of caspase-3 activity and western blotting were used to detect cellular proliferation, migration and adhesion, caspase-3 activity, and Bax and Bcl-2 protein expression, respectively, in GBM cells. The results of the present study demonstrated that RFC2 expression was increased in GBM tissues and cell lines. Overexpression of RFC2 promoted cellular proliferation, migration, adhesion and an increase in Bcl-2 protein levels, and suppressed cellular caspase-3 activity and Bax protein expression, while silencing RFC2 resulted in the opposite effect. The effects of miR-744-5p inhibition were similar to those of RFC2 overexpression. Moreover, miR-744-5p was found to target RFC2 in GBM cells, and inhibiting the expression of RFC2 suppressed GBM tumorigenesis. In conclusion, the present study demonstrated that miR-744-5p targets RFC2 and suppresses the progression of GBM by repressing cellular proliferation, migration and Bcl-2 protein expression, and effectively promoting caspase-3 activity and Bax protein expression. These findings suggest a new target for the clinical treatment and improved prognosis of patients with GBM in the future.

Project description:BackgroundCircular RNAs (circRNAs) are increasingly implicated in regulating human carcinogenesis. Previous work showed the oncogenic activity of circ_0018289 in cervical cancer. However, the molecular basis underlying the modulation of circ_0018289 in cervical carcinogenesis is still not fully understood.MethodsThe levels of circ_0018289, microRNA (miR)-183-5p, and transmembrane p24 trafficking protein 5 (TMED5) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Ribonuclease (RNase) R and subcellular localization assays were used to characterize circ_0018289. Cell proliferation was detected by the Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (Edu) assays. Cell apoptosis and tube formation were assessed by flow cytometry and tube formation assays, respectively. A dual-luciferase reporter assay was performed to confirm the direct relationship between miR-183-5p and circ_0018289 or TMED5. The role of circ_0018289 in tumor growth was gauged by mouse xenograft experiments.ResultsCirc_0018289 was overexpressed in cervical cancer tissues and cells. Circ_0018289 silencing impeded cell proliferation, enhanced cell apoptosis, and suppressed angiogenesis in vitro, as well as diminished tumor growth in vivo. Mechanistically, circ_0018289 targeted and regulated miR-183-5p by binding to miR-183-5p, and circ_0018289 regulated cervical cancer development and angiogenesis partially through miR-183-5p. Moreover, TMED5 was directly targeted and inhibited by miR-183-5p through the perfect complementary sites in TMED5 3'UTR, and TMED5 knockdown phenocopied miR-183-5p overexpression in suppressing cervical cancer development and angiogenesis. Furthermore, circ_0018289 induced TMED5 expression by competitively binding to shared miR-183-5p.ConclusionOur observations identified the circ_0018289/miR-183-5p/TMED5 regulatory network as a novel molecular basis underlying the modulation of cervical carcinogenesis.

Dataset Information

MicroRNA-183-5p Inhibits Aggressiveness of Cervical Cancer Cells by Targeting Integrin Subunit Beta 1 (ITGB1).

Publications

MicroRNA-183-5p Inhibits Aggressiveness of Cervical Cancer Cells by Targeting Integrin Subunit Beta 1 (ITGB1).

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