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MiR?185?5p inhibits F?actin polymerization and reverses epithelial mesenchymal transition of human breast cancer cells by modulating RAGE.

ABSTRACT: In our previous study, advanced glycosylation end?product specific receptor (RAGE) was observed to bind to S100A8/A9 and cause epithelial mesenchymal transition (EMT). The results from target gene prediction revealed that microRNA (miR)?185?5p had a RAGE binding site. However, the function of miR?185?5p in the invasion and migration of breast cancer remains ambiguous. In the present study, the expression of miR?185?5p was examined in breast cancer tissues and cells. Clinical features revealed a negative correlation between miR?185?5p and tumor size, as well as in tumor differentiation and lymph node metastasis in breast cancer. In addition, miR?185?5p was negatively associated with RAGE, and this miRNA reversed the EMT of breast cancer by modulating RAGE in vitro. In addition, miR?185?5p inhibited the S100A8/A9?induced EMT of breast cancer cells by the nuclear factor??B/Snail signaling pathway. Notably, miR?185?5p upregulation inhibited the F?actin polymerization induced by S100A8/A9 in breast cancer. Furthermore, overexpression of miR?185?5p and reduction of RAGE inhibited lung metastasis node in vivo. Thus, miR?185?5p represents a potential therapeutic target in breast cancer by modulating RAGE.

SUBMITTER: Yin C

PROVIDER: S-EPMC6102692 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature

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miR‑185‑5p inhibits F‑actin polymerization and reverses epithelial mesenchymal transition of human breast cancer cells by modulating RAGE.

Yin Chonggao C Zhang Guoxin G Sun Ruimei R Pan Xinting X Wang Xuewen X Li Hongli H Sun Yunbo Y

Molecular medicine reports 20180716 3

In our previous study, advanced glycosylation end‑product specific receptor (RAGE) was observed to bind to S100A8/A9 and cause epithelial mesenchymal transition (EMT). The results from target gene prediction revealed that microRNA (miR)‑185‑5p had a RAGE binding site. However, the function of miR‑185‑5p in the invasion and migration of breast cancer remains ambiguous. In the present study, the expression of miR‑185‑5p was examined in breast cancer tissues and cells. Clinical features revealed a ...[more]

PMID: 30015912

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Project description:BackgroundGlioma metastasis, invasion, epithelial-mesenchymal transition (EMT) and chemoresistance indicate poor prognosis. Accumulating evidence reveals that Notch1 is an important factor in tumour progression. However, the role of Notch1 in glioma EMT and associated microRNAs (miRNAs) with the Notch pathway remain controversial.MethodsUtilizing cBioPortal database to examine the gene signature of NOTCH1 (encoding Notch1), CDH2 (encoding N-cadherin) and SNAI1 (encoding Snail-1) in disease-free survival (DFS) and overall survival (OS). We analyzed the Notch1 expression from Oncomine. We used Western blot (WB), immunohistochemistry (IHC) and immunofluorescence to determine protein levels. Transcription was evaluated by quantitative real-time (qRT)-PCR. siRNA and lentivirus were used to knock down Notch1 and overexpress miR-139-5p, respectively. The migration and invasion of glioma cells were assessed by wound healing and transwell assays. Luciferase reporter assays were utilized to verify the relationship between Notch1 and miR-139-5p. A U87-implanted intracranial model was used to study the effect of miR-139-5p on tumour growth and Notch1 suppression efficacy or EMT reversion.ResultsIt revealed the association of NOTCH1, CDH2, SNAI1 genomic alterations with decreases in DFS and OS. Notch1 was upregulated in classical and proneural subtypes of GBM, and associated with tumour grade. Notch1 inhibition suppressed the biological behaviours of metastasis, invasion and EMT. Notch1 was identified as a novel direct target of miR-139-5p. MiR-139-5p overexpression partially phenocopied Notch1 siRNA, whereas the forced expression of Notch1 reversed the effects of miR-139-5p on the invasion of glioma. Moreover, intracranial tumourigenicity and EMT behaviours were reduced by the introduction of miR-139-5p and partially mediated by the decreased Notch1 expression.ConclusionsmiR-139-5p was identified as a tumour suppressor by negatively targeting Notch1, and this work suggests a possible molecular mechanism of the miR-139/Notch1/EMT axis for glioma treatment.

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MiR?185?5p inhibits F?actin polymerization and reverses epithelial mesenchymal transition of human breast cancer cells by modulating RAGE.

Publications

miR‑185‑5p inhibits F‑actin polymerization and reverses epithelial mesenchymal transition of human breast cancer cells by modulating RAGE.

Similar Datasets

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