Circular RNA CEP128 Promotes Bladder Cancer Progression by Regulating Mir-145-5p/Myd88 Via Mapk Signaling Pathway.

08:00 EDT 2nd April 2019 | BioPortfolio

Summary of "Circular RNA CEP128 Promotes Bladder Cancer Progression by Regulating Mir-145-5p/Myd88 Via Mapk Signaling Pathway."

The present experiment was designed for exploring the regulatory mechanism of circ-CEP128/miR-145-5p/MYD88 axis in bladder cancer. MiRNAs and circRNAs expression data were derived from Gene Expression Omnibus database (GEO) with bladder tumor tissues and para-carcinoma tissue samples. Differentially expressed genes (DEGs) in tumor were analyzed via R software. Interaction network of differently expressed miRNAs and differently expressed mRNA was established by means of Cytoscape software. CircCEP128 and miR-145-5p expression levels were determined using qRT-PCR. The expression of MAPK signaling-related proteins MYD88, p38, ERK and JNK was examined by western blot. The relationship between circCEP128 and miR-145-5p was validated using RNA immunoprecipitation. The level of cell propagation and migration was determined by CCK8 and wound healing assay, BrdU assay and migration assay. Cell apoptosis rate and cell cycle were detected via flow cytometry. Tumor xenograft assay was implemented to investigate the function of circCEP128 in vivo. CircCEP128 and MYD88 were overexpressed in bladder cancer based on microarray analysis and miR-145-5p was a potential targeting factor in bladder cancer. CircCEP128 targeted miR-145-5p and miR-145-5p targeted MYD88. Expression of miR-145-5p was decreased in cancer samples. Knockdown of circCEP128 induced the inhibition of cell viability and mobility and cell cycle arrest. Overexpression of miR-145-5p or knockdown of circCEP128 promoted MAKP signaling pathway and related proteins expression. In addition, knockdown of circCEP128 suppressed the growth of bladder cancer tumor tissues in vivo. Overexpression of circCEP128 promoted bladder cancer progression through modulating miR-145-5p and MYD88 via MAKP signaling pathway. This article is protected by copyright. All rights reserved.


Journal Details

This article was published in the following journal.

Name: International journal of cancer
ISSN: 1097-0215


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