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MiRNA-335 and miRNA-182 affect the occurrence of tongue squamous cell carcinoma by targeting survivin.

ABSTRACT: The aim of the present study was to characterize the roles of two microRNAs (miRs) that have been reported to be differentially expressed in tongue squamous cell carcinoma (TSCC), miR-335 and miR-182. In total, 20 tumor tissue samples and 20 corresponding adjacent non-cancerous samples were collected from patients with TSCC to measure the expression of miR-335 and miR-182 and the potential shared target of these miRs, survivin, using reverse transcription-quantitative polymerase chain reaction and western blotting. In the TSCC tissue samples, significantly decreased expression of the two miRs and increased expression of survivin were detected compared with adjacent non-cancerous controls. Subsequently, it was confirmed that survivin was the target gene of miR-335 and miR-182 using a luciferase assay in TSCC cells. In order to examine the function of miR-335 and miR-182 in the development of TSCC, TSCC cells were transiently transfected with the mimics of the two miRs, and it was confirmed that the introduction of miR-335 and miR-182 to cells suppressed the expression of survivin and markedly inhibited the proliferation of the TSCC cells. Furthermore, miR-335 and miR-182 were found to induce cell cycle arrest by suppressing the expression of survivin. The present study revealed a negative regulatory role of miR-335 and miR-182 in the proliferation of TSCC cells by targeting survivin, and miR-335 and miR-182 may be novel therapeutic targets for the treatment of TSCC.

SUBMITTER: Ou D

PROVIDER: S-EPMC5038158 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature

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miRNA-335 and miRNA-182 affect the occurrence of tongue squamous cell carcinoma by targeting survivin.

Ou Deming D Wu Ying Y Liu Jun J Lao Xiaomei X Zhang Sien S Liao Guiqing G

Oncology letters 20160803 4

The aim of the present study was to characterize the roles of two microRNAs (miRs) that have been reported to be differentially expressed in tongue squamous cell carcinoma (TSCC), miR-335 and miR-182. In total, 20 tumor tissue samples and 20 corresponding adjacent non-cancerous samples were collected from patients with TSCC to measure the expression of miR-335 and miR-182 and the potential shared target of these miRs, survivin, using reverse transcription-quantitative polymerase chain reaction a ...[more]

PMID: 27698823

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Project description:Background:MicroRNA27b-3p (miR-27b) has been reported to be dysregulated in multiple types of human cancer. However, the expression levels, biological roles, and underlying mechanism of miR-27b in tongue squamous cell carcinoma (TSCC) remain to be elucidated. Methods:Bioinformatics analyses and quantitative real-time PCR (qRT-PCR) were used to determine miR-27b expression in TSCC tissues and cell lines. The influence of miR-27b overexpression or inhibition on TSCC cell proliferation, migration, and invasion in vitro, and on tumor growth in vivo, was explored via CCK8, colony formation, wound healing, and transwell assays, and in xenograft tumors in nude mice, respectively. Luciferase reporter assays, qRT-PCR, and Western blotting were performed to clarify the potential mechanisms involving miR-27b in TSCC cells. Results:miR-27b was significantly downregulated in TSCC tissues and cell lines, and its expression was correlated with cancer status. Overexpression of miR-27b led to diminished proliferation, migration, and invasion, and notably reduced tumor growth in vivo. Bioinformatics analysis followed by luciferase reporter assays demonstrated that miR-27b expression was inversely correlated with that of integrin subunit ?5 (ITGA5)and that miR-27b directly bound to the 3'-untranslated region of ITGA5 in TSCC cells. The bioinformatics analysis also indicated that ITGA5 was upregulated in TSCC and that its expression was correlated with epithelial-mesenchymal transition (EMT) and poor prognosis. Moreover, we found that miRNA-27b could reverse ITGA5-induced promotion of TSCC cell proliferation and migration. Finally, we demonstrated that regulation of miR-27b expression in TSCC may result in alterations in the expression of ITGA5 and EMT-related marker genes at the mRNA and protein levels. Conclusion:These results indicate that miR-27b hampers TSCC proliferation and migration via suppressing the EMT process by targeting ITGA5. These findings support consideration of miR-27b/ITGA5 as a valuable marker for the metastatic potential of TSCC, or as a therapeutic target for the treatment of TSCC.

Project description:This study demonstrated that miR‐335‐5p expression was reduced in HNSCC. miR‐335‐5p expression could inhibit HNSCC cell growth, metastasis, and promote cell apoptosis while it could suppress tumor growth in vivo. We identified MAP3K2 as a novel target of miR‐335‐5p and MAP3K2 overexpression partially rescued the inhibitory role of miR‐335‐5p. Hence, miR‐335‐5p might constitute a potential therapeutic target for HNSCC patients. Mounting evidence has indicated that aberrantly expressed microRNAs (miRNAs) play key roles in tumorigenesis, including in head and neck squamous cell carcinoma (HNSCC). Previous studies have shown that miR‐335‐5p can serve as a tumor suppressor or an oncogene in cancer. However, the clinical importance and biological effects of miR‐335‐5p in HNSCC have not been determined. Here, we investigated the expression pattern, functional role, and mechanisms of miR‐335‐5p in HNSCC. We showed a decreased expression of miR‐335‐5p in HNSCC samples from the TCGA and GEO databases. Consistently, we detected a downregulation of miR‐335‐5p in HNSCC cell lines and patient tissues. The expression of miR‐335‐5p was inversely correlated with advanced clinical TNM stage and lymph node metastasis in HNSCC patients. miR‐335‐5p overexpression inhibited HNSCC cell proliferation and induced apoptosis, while miR‐335‐5p inhibition had the opposite effects. miR‐335‐5p overexpression suppressed tumor growth in mice. Bioinformatic analyses and functional assays identified MAP3K2 as a target of miR‐335‐5p, and we showed that miR‐335‐5p downregulated mitogen‐activated protein kinase kinase kinase 2 (MAP3K2) expression in HNSCC cells. We found an inverse association between MAP3K2 and miR‐335‐5p expression in 38 pairs of HNSCC tissues. Furthermore, the effect of miR‐335‐5p overexpression on growth and metastasis as well as cell apoptosis in HNSCC cells could be partially rescued by MAP3K2 expression. Collectively, our data show that miR‐335‐5p inhibits the development of HNSCC by regulating MAP3K2 expression. Thus, these findings offer novel insights into a potential therapeutic strategy for HNSCC patients.

Dataset Information

MiRNA-335 and miRNA-182 affect the occurrence of tongue squamous cell carcinoma by targeting survivin.

Publications

miRNA-335 and miRNA-182 affect the occurrence of tongue squamous cell carcinoma by targeting survivin.

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