Dataset Information

MicroRNA-495 downregulates FOXC1 expression to suppress cell growth and migration in endometrial cancer.

ABSTRACT: MicroRNAs (miRNAs) are a class of noncoding RNAs and function as key regulators of gene expression at the post-transcriptional level. In this study, we found that miR-495 reduces cell growth, induces apoptosis and suppresses the migration of endometrial cancer by directly inhibiting FOXC1 expression. Further analysis revealed that FOXC1 promotes growth and migration and functions as an oncogene in vitro. FOXC1 overexpression reversed the cellular responses mediated by miR-495 in endometrial cancer cells. We also found that miR-495 suppresses the growth of endometrial cancer in vivo. Altogether, these results indicate that miR-495 acts as a tumour suppressor gene by targeting FOXC1 at the post-transcriptional level in endometrial cancer.

SUBMITTER: Xu YY

PROVIDER: S-EPMC4841847 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature

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MicroRNA-495 downregulates FOXC1 expression to suppress cell growth and migration in endometrial cancer.

Xu Yan-Ying YY Tian Jing J Hao Quan Q Yin Li-Rong LR

Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 20150722 1

MicroRNAs (miRNAs) are a class of noncoding RNAs and function as key regulators of gene expression at the post-transcriptional level. In this study, we found that miR-495 reduces cell growth, induces apoptosis and suppresses the migration of endometrial cancer by directly inhibiting FOXC1 expression. Further analysis revealed that FOXC1 promotes growth and migration and functions as an oncogene in vitro. FOXC1 overexpression reversed the cellular responses mediated by miR-495 in endometrial canc ...[more]

PMID: 26198045

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Project description:Osteoblasts are implicated in the building of the vertebrate skeleton. The current study aimed to investigate the role of microRNA-495 (miR-495) in the osteoblasts of mice with tibial fractures and the underlying mechanism involving in aquaporin-1 (AQP1) and the p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway. Initially, a microarray-based analysis was performed to screen the differentially expressed genes and miRNAs associated with tibial fracture. Following the establishment of a tibial fracture mouse model, the positive rate of the AQP1 protein in the fracture tissue was detected by immunohistochemistry (IHC). Next, to verify the binding site between miR-495 on AQP1, bioinformatics data were employed in addition to the application of a dual-luciferase reporter gene assay. The osteoblast cell line MC3T3-E1 was treated with miR-495 mimic, miR-495 inhibitor and Anisomycin to explore the potent effects of miR-495 on proliferation and differentiation of osteoblasts in mice with tibial fracture. The expression of miR-495, AQP1, p38 MAPK, PCNA, Cyclin D1, OCN, and OPN was subsequently evaluated by RT-qPCR and Western blot analysis. Cell viability, the number of calcium nodules and alkaline phosphatase (ALP) activity were detected by MTT assay, alizarin red staining, and ALP activity assay, respectively. Our results revealed that miR-495 was down-regulated while AQP1 was up-regulated in the mice with tibial fractures. AQP1 was verified as a target gene of miR-495. When the cells were treated with overexpressed miR-495 or activated p38 MAPK signaling pathway, elevated expression of PCNA, Cyclin, D1, OCN, and OPN along with an increased amount of calcium nodules, higher cell viability, and enhanced ALP activity was detected, while the expression of AQP1 was reduced. Collectively, the key findings of the present study support the notion that overexpressed miR-495 may activate the p38 MAPK signaling pathway to inhibit AQP1 and to promote the proliferation and differentiation of osteoblasts in mice with tibial fracture.

Dataset Information

MicroRNA-495 downregulates FOXC1 expression to suppress cell growth and migration in endometrial cancer.

Publications

MicroRNA-495 downregulates FOXC1 expression to suppress cell growth and migration in endometrial cancer.

Similar Datasets

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