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Chronic stress promotes EMT-mediated metastasis through activation of STAT3 signaling pathway by miR-337-3p in breast cancer

ABSTRACT: The aim of this research is to explore the metastasis associated negative effect of chronic stress. The analysis of transcriptome sequencing implied that activation of STAT3 signaling pathway by miR-337-3p might be a potential mechanism to induce epithelial to mesenchymal transition (EMT) of cancer cell and promote metastasis under chronic stress. We also verified this biological process in further experiments. Downregulation of miR-337-3p could downregulate E-cadherin expression and upregulate vimentin expression in vitro and in vivo. STAT3, related signal pathways of which are involved in metastasis regulation, was directly targeted by miR-337-3p.

ORGANISM(S): Mus musculus

PROVIDER: GSE154685 | GEO | 2021/07/20

REPOSITORIES: GEO

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Project description:The regulation of gene expression in cells, including by microRNAs (miRNAs), is a dynamic process. Current methods for identifying microRNA targets by combining sequence, miRNA and mRNA expression data do not adequately utilize the temporal information and thus miss important miRNAs and their targets. We developed a new method, mirDREM, that uses probabilistic modeling to reconstruct dynamic regulatory networks which explain how temporal gene expression is jointly regulated by microRNAs and transcription factors (TFs). We used mirDREM to study the regulation of postnatal lung development in mice. The reconstructed network for this process identified several known miRNAs and TFs and provided novel predictions about additional miRNAs and the specific developmental phases they regulate. Microarray data of Mouse Lung Epithelial cells MLE-12 after transfection with inhibitors for miR-30a, miR-30d, miR-23b and miR-125 and with precursors for miR-337, miR-466a, miR466d and miR-476c. The results provide a general insight into the gene expression profile which was modulated by the inhibition or overexpression of these microRNAs. We experimentally validated several predictions and show that miR-30d, miR-30a, and miR-467c are new regulators of proliferation in lung cells. Our analysis establishes new links between identified miRNAs and lung diseases, supporting recent evidence that such diseases may represent reversal of lung differentiation. We first analyzed the endogenous expression of miR-30a, miR-30d, miR-23b, miR-125, miR-337, miR-466a, miR466d and miR-476c in MLE-12 cells. Then, we transfected the MLE-12 cells with inhibitors ( miR-30a, miR-30d, miR-23b and miR-125) for the highly expressed and precursos for those that were almost undetectable (miR-337, miR-466a, miR466d and miR-476c). RNA level of the 8 microRNAs was verify by qRT-PCR in order to validate the transfection efficiency. Finally, 0.5ug of total RNA was used to performe the gene expression microarrays for each condition

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Chronic stress promotes EMT-mediated metastasis through activation of STAT3 signaling pathway by miR-337-3p in breast cancer

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