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RNA-Seq analysis miR-455-3p overexpression effect on breast cancer cell line

ABSTRACT: MiR-455-3p has been reported to suppress the expression of ROCK2, HOXB5, hTERT, and RUNX2, which are involved in multiple biological processes including renal fibrosis, chondrogenic development and differentiation, Alzheimer’s disease, preeclampsia, and tumorigenesis. Here, we showed that miR-455-3p broadly inhibited TGF-beta-induced EMT by repressing the expression of Smad2, ZEB1, and HDAC2 in breast cancer cells, and that miR-455-3p loss-of-function promotes the acquisition of cell invasive properties and the ability to metastasize. These results indicate that miR-455-3p represents an important node that inhibits metastasis of breast cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE129146 | GEO | 2019/09/06

REPOSITORIES: GEO

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Project description:MicroRNAs (miRNAs, micro ribonucleic acids) are pivotal post-transcriptional regulators of gene expression. These endogenous small non-coding RNAs play significant roles in tumorigenesis and tumor progression. miR-142-3p expression is dysregulated in several breast cancer subtypes. We aimed at investigating the role of miR-142-3p in breast cancer cell invasiveness. Supported by transcriptomic Affymetrix array analysis and confirmatory investigations at the mRNA and protein level, we demonstrate that overexpression of miR-142-3p in MDA-MB-231, MDA-MB-468 and MCF-7 breast cancer cells leads to downregulation of WASL (Wiskott-Aldrichsyndrome-like, protein: N-WASP), Integrin-aV, RAC1, and CFL2, molecules implicated in cytoskeletal regulation and cell motility. ROCK2, IL6ST, KLF4, PGRMC2 and ADCY9 were identified as additional targets in a subset of cell lines. Decreased matrigel invasiveness was associated with the miR-142-3p-induced expression changes. Confocal immunofluorescence microscopy, nanoscale atomic force microscopy and digital holographic microscopy revealed a change in cell morphology as well as a reduced cell volume and size. A more cortical actin distribution and a loss of membrane protrusions were observed in cells overexpressing miR-142-3p. Luciferase activation assays confirmed direct miR-142-3p-dependent regulation of the 3'-untranslated region of ITGAV and WASL. siRNA-mediated depletion of ITGAV andWASL resulted in a significant reduction of cellular invasiveness, highlighting the contribution of these factors to the miRNA-dependent invasion phenotype. While knockdown of WASL significantly reduced the number of membrane protrusions compared to controls, knockdown of ITGAV resulted in a decreased cell volume, indicating differential contributions of these factors to the miR-142-3p-induced phenotype. Our data identify WASL, ITGAV and several additional cytoskeleton associated molecules as novel invasion-promoting targets of miR-142-3p in breast cancer.

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RNA-Seq analysis miR-455-3p overexpression effect on breast cancer cell line

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