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MicroRNA-328 inhibits migration and epithelial-mesenchymal transition by targeting CD44 in nasopharyngeal carcinoma cells.

ABSTRACT: Background:MicroRNAs (miRNAs) play crucial roles in various types of cancers, particularly in tumor development, migration, and progression. Dysregulation of miR-328 was reported to occur in some types of human malignancies, however, the role of miR-328 in nasopharyngeal carcinoma (NPC) and its potential involvement in metastasis remain undetermined. Methods:The invasion capacity of NPC sphere-forming cells was evaluated by in vitro cell migration assays. Differential miRNAs expression was examined in NPC sphere-forming cells compared to parental monolayer cells using miRNA array analysis. The role of miR-328 in regulating NPC cells migratory properties was analyzed after miR-328 mimics transfection. The expression of E-cadherin and CD44 was analyzed by flow cytometry. CD44 was examined as a target of miR-328 through luciferase reporter assays and Western blotting. Results:Here, we report that NPC TW01 and TW06 sphere-forming cells exhibited increased migratory ability in comparison with parental monolayer cells. Sphere-forming cells had significantly lower levels of miR-328, as observed using miRNA arrays and confirmed through real-time polymerase chain reaction. Overexpression of miR-328 induced by transfection with synthetic miR-328 mimics decreased the migration of NPC sphere-forming cells. The inhibitory effects were associated with increased expression of E-cadherin and the downregulated expression of mesenchymal markers such as N-cadherin, Snail, and vimentin. Moreover, our results demonstrated that miR-328 suppressed NPC cell migration and inhibited the epithelial-mesenchymal transition process directly through a binding site on the CD44 3' untranslated region. Conclusion:miR-328, a previously unrecognized miRNA, may serve as a potential prognostic marker and therapeutic target for NPC.

SUBMITTER: Lin CH

PROVIDER: S-EPMC5931237 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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MicroRNA-328 inhibits migration and epithelial-mesenchymal transition by targeting CD44 in nasopharyngeal carcinoma cells.

Lin Chien-Hung CH Chiang Ming-Chang MC Chen Yann-Jang YJ

OncoTargets and therapy 20180427

<h4>Background</h4>MicroRNAs (miRNAs) play crucial roles in various types of cancers, particularly in tumor development, migration, and progression. Dysregulation of miR-328 was reported to occur in some types of human malignancies, however, the role of miR-328 in nasopharyngeal carcinoma (NPC) and its potential involvement in metastasis remain undetermined.<h4>Methods</h4>The invasion capacity of NPC sphere-forming cells was evaluated by in vitro cell migration assays. Differential miRNAs expre ...[more]

PMID: 29740213

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Project description:Metastasis is responsible for the rapid recurrence and poor survival of malignancies. Epithelial-mesenchymal transition (EMT) has a critical role in metastasis. Increasing evidence indicates that EMT can be regulated by microRNAs (miRNAs). The aim of this study was to investigate the role of miR-26b in modulating epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC), as well as to identify its underlying mechanism of action.The expression level of miR-26b was assessed in multiple HCC cell lines (HepG2, MHCC97H, Hep3B, MHCC97L, HCCC9810, BEL-7402, Huh7 and QGY-7703), as well as in liver tissue from patients with HCC. Follow-up studies examined the effects of a miR-26b mimic (increased expression) and a miR-26b inhibitor (decreased expression) on markers of EMT, wound healing and cell migration. The molecular target of miR-26b was also identified using a computer algorithm and confirmed experimentally.MiR-26b expression was decreased in HCC cell lines and was inversely correlated with the grade of HCC. Increased expression of miR-26b inhibited the migration and invasiveness of HCC cell lines, which was accompanied by decreased expression of the epithelial marker E-cadherin and increased expression of the mesenchymal marker vimentin, at both the mRNA and protein expression levels. A binding site for miR-26b was theoretically identified in the 3'UTR of USP9X. Further studies revealed that overexpression of miR-26b repressed the endogenous level of USP9X protein expression. Overexpression of miR-26b also repressed Smad4 expression, whereas its inhibition elevated Smad4 expression.Taken together, our results indicate that miR-26b were inhibited in HCC. In HCC cell lines, miR-26b targeted the 3'UTR of USP9X, which in turn affects EMT through Smad4 and the TGF-? signaling pathway. Our analysis of clinical HCC samples verifies that miR-26b also targets USP9X expression to inhibit the EMT of hepatocytes. Thus, miR-26b may have some effects on the EMT of HCC cells.

Project description:ObjectiveGlioma has the highest incidence among the different tumor types within the nervous system, accounting for about 40% of them. Malignant glioma has a high invasion and metastasis rate, which leads to the poor prognosis of patients. By targeting specific genes, microRNAs serve as key regulators in the epithelial-mesenchymal transformation (EMT) process, which could provide new insights into the treatment of glioblastomas (GBM). The detailed molecular role that miR-623 plays in GBM still remains unclear.Materials and methodsThe level of miR-623 in GBM cells was evaluated by RT-PCR. The function of miR-623 overexpression on GBM cell proliferation, migration, and invasion was assessed by MTS, Transwell analysis, and colony formation assay. In addition, a mouse subcutaneous xenograft model was used to study in vivo effects. The binding between miR-623 and TRIM44 was verified by a dual-luciferase reporter assay and the regulatory function of miR-623 on EMT markers was evaluated using Western blot.ResultsThe expression of miR-623 was repressed in the GBM cancer cell lines. MiR-623 overexpression or TRIM44 knockdown attenuated the proliferation, migration, and invasion of GBM cell lines. TRIM44 could facilitate the reverse suppression of EMT and miR-623 in GBM progression. MiR-623 was found to inhibit TRIM44 expression by directly binding to its 3'UTR. In addition, systemic delivery of miR-623 mimic reduced tumor growth and inhibited TRIM44 protein expression in tumor-bearing nude mice. Furthermore, our findings indicated that miR-623 overexpression or TRIM44 down-regulation impeded the proliferation and migratory ability of LN229 and U251MG glioma cells, and miR-623 attenuates TRIM44-induced EMT by directly targeting the 3'UTR of TRIM44, which could serve as preliminary research to identify potential therapeutic targets for future treatment of GBM.ConclusionOverall, microRNA-623 inhibits epithelial-mesenchymal transition to attenuate glioma proliferation by targeting TRIM44.

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MicroRNA-328 inhibits migration and epithelial-mesenchymal transition by targeting CD44 in nasopharyngeal carcinoma cells.

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MicroRNA-328 inhibits migration and epithelial-mesenchymal transition by targeting CD44 in nasopharyngeal carcinoma cells.

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