Dataset Information

MiR-506 is a YAP1-dependent tumor suppressor in laryngeal squamous cell carcinoma.

ABSTRACT: Laryngeal squamous cell carcinoma (LSCC) accounts for 95% of laryngeal cancer incidence. Tobacco use has been shown to have a linear association with the development of the disease. While early diagnosis and treatment of LSCC are critical in improving the 5-year survival rate and quality of life, diagnosis of early-stage LSCC remains challenging because of the unapparent symptoms. Here, we report that miR-506, a critical regulator in many types of cancers, is aberrantly suppressed in LSCC patient tissues and cultured cancer cells. This is likely responsible for the enhanced production of YAP1 protein, a transcriptional factor that is well known for its oncogenic roles in LSCC malignancy. Statistical analysis has confirmed that the expression levels of miR-506 and YAP1 are strongly correlated with the malignant statuses of patient tumors. Restoring the expression level of miR-506 in cultured LSCC cells significantly inhibited proliferation, migration and invasion of the cells. The miR-506 and YAP1 regulatory network seems to affect at least pathways involved in apoptosis. Our study, for the first time, has demonstrated a tumor suppressive role of miR-506 in LSCC. This opens new opportunities for further exploring the molecular details of the development of the disease and thus will facilitate the development of novel diagnosis and therapeutic strategies.

SUBMITTER: Gao C

PROVIDER: S-EPMC6606012 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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miR-506 is a YAP1-dependent tumor suppressor in laryngeal squamous cell carcinoma.

Gao Changhui C Hu Shousen S

Cancer biology & therapy 20190325 6

Laryngeal squamous cell carcinoma (LSCC) accounts for 95% of laryngeal cancer incidence. Tobacco use has been shown to have a linear association with the development of the disease. While early diagnosis and treatment of LSCC are critical in improving the 5-year survival rate and quality of life, diagnosis of early-stage LSCC remains challenging because of the unapparent symptoms. Here, we report that miR-506, a critical regulator in many types of cancers, is aberrantly suppressed in LSCC patien ...[more]

PMID: 30907227

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Project description:PurposeLong noncoding RNAs (lncRNAs) have been identified as an important class of noncoding RNAs that are deeply involved in multiple biological processes in tumorigenesis. This study is to investigate the critical roles and biological function of lncRNA growth arrest-specific 5 (GAS5) in tumorigenesis of laryngeal squamous cell carcinoma (LSCC).Patients and methodsA total of 59 samples of LSCC and paired adjacent tissue, as well as corresponding clinicopathological information were collected. GAS5 expression in both LSCC tissues and human SUN1076 and SNU899 cell lines were analyzed by Real-time quantitative RT-PCR method. Ectopic expression of GAS5 by vector transfection in LSCC cell lines and followed by in vitro experiments was to investigate the critical roles and function of GAS5 in LSCC. Cell Counting Kit 8 (CCK8) assay and PE/7AAD Annexin V Apoptosis analysis was to evaluate cell proliferation ability and cell apoptosis. Co-transfection of GAS5 and miR-21 was to explore the interaction between GAS5 and miR-21 in LSCC. BAX and CDK6 protein level were analyzed by western blot method.ResultsThis study demonstrated that GAS5 was significantly downregulated in LSCC tissue and human LSCC cell lines. GAS5 levels were correlated with the clinicopathological features of LSCC patients. In addition, the ectopic expression of GAS5 significantly inhibited cell proliferation and promoted apoptosis. Co-expression analyses indicated that GAS5 is negatively correlated with miR-21 in LSCC tissues. Overexpression of miR-21 eliminated GAS5-mediated cell apoptosis and proliferation suppression. Furthermore, GAS5, which upregulated BAX mRNA expression and downregulated CDK6 mRNA expression, was reversed by ectopic expression of miR-21.ConclusionGAS5 suppresses LSCC progression through the negative regulation of miR-21 and its targets involved in cell proliferation and apoptosis, indicating that GAS5 may serve as a biomarker and potential target for LSCC therapy.

Project description:BackgroundTo study miR-30b-5p expression in esophageal squamous cell carcinoma (ESCC) by comparisons between tumor tissues and matched adjacent non-cancerous tissues to elucidate the correlation between miR-30b-5p expression and ESCC clinical parameters, and to explore the signaling pathways associated with miR-30b-5p and key target genes.MethodsClinical data, cancer tissues, and adjacent non-cancerous tissues of 32 patients diagnosed with ESCC were collected from Taizhou Hospital of Zhejiang Province. The expression levels of miR-30b-5p were determined by real-time polymerase chain reaction (RT-PCR). mRNA data for ESCC tissues and normal tissues, and clinical materials of patients with ESCC were obtained from the Gene Expression Omnibus (GEO) database and The Cancer Genome Atlas (TCGA). Associations between miR-30b-5p expression and clinical features of patients with ESCC and overall survival were explored. A bioinformatics analysis was performed to determine the pathways and key miR-30b-5p targets associated with ESCC. Additionally, a cytological experiment was performed to evaluate the biological functions of miR-30b-5p. Finally, correlations between miR-30b-5p and key targets involved in PI3K/Akt signaling pathways were validated by western blotting.ResultsThe expression level of miR-30b-5p in the 32 ESCC tissues was significantly lower than that in adjacent normal tissues (P<0.01) and was significantly disparate in the T stage, with higher expression in T1 than in T2 (P<0.05). Among the patients with higher expression levels of miR-30b-5p in ESCC tissues than in adjacent normal tissues, patients with higher expression of miR-30b-5p had a better prognosis (P<0.05). An analysis of gene chip data from the GEO database showed similar results. A gene enrichment analysis indicated a series of pathways that may be associated with the downregulation of miR-30b-5p, including focal adhesion, ECM-receptor interaction, and PI3K/Akt signaling pathways. Seven key target genes (PDGFRB, VIM, ITGA5, ACTN1, THBS2, SERPINE1, and RUNX2) were identified; these were found to be upregulated in ESCC tissues and were negatively correlated with miR-30b-5p. Functional experiments showed that miR-30b-5p attenuated migration (P<0.01) and invasion (P<0.05) in the Eca109 cell line. Moreover, the levels of ITGA5, PDGFRB, p-PI3K, and p-AKT, which are involved in the PI3K/Akt signaling pathway, were decreased in the miR-30b-5p-overexpressing Eca109 cell line.ConclusionsUpregulated miR-30b-5p may inhibit migration and invasion in ESCC by targeting ITGA5, PDGFRB, and signaling pathways, such as PI3K/Akt, involved in ESCC regulation. Our results indicate that miR-30b-5p plays an important role in the occurrence and progression of ESCC and is a potential therapeutic target.

Dataset Information

MiR-506 is a YAP1-dependent tumor suppressor in laryngeal squamous cell carcinoma.

Publications

miR-506 is a YAP1-dependent tumor suppressor in laryngeal squamous cell carcinoma.

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