Dataset Information

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:Objective:Glioma 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 Methods:The 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. Results:The 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. Conclusion:Overall, 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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