ArticleMolecular biology of the cell2024
mDia2 is an important mediator of MRTF-A-dependent regulation of breast cancer cell migration.
Article in Molecular biology of the cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- P95-HER2 promotes metastatic progression by biasing MRTFA dependent signaling.bioRxiv : the preprint server for biology · 2026Article
- LamelliQuant: An Automated Analysis Pipeline for Lamellipodia Protrusion Dynamics.Cytoskeleton (Hoboken, N.J.) · 2026Article
- Breast cancer cells promote osteoclast differentiation in an MRTF-dependent paracrine manner.Molecular biology of the cell · 2025Article
- DIAPH3 is upregulated in high-grade gliomas and linked to chromosomal instability.Neuro-oncology advancesArticle
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Abstract
Dysregulated actin cytoskeleton gives rise to aberrant cell motility and metastatic spread of tumor cells. This study evaluates the effect of overexpression of wild-type versus functional mutants of MRTF-A on migration and invasion of breast cancer (BC) cells. Our studies indicate that SRF's interaction is critical for MRTF-A-induced promotion of both two-dimensional and three-dimensional cell migration, while the SAP-domain function is important selectively for three-dimensional cell migration. Increased MRTF-A activity is associated with more effective membrane protrusion, a phenotype that is attributed predominantly to SRF's interaction with MRTF. We demonstrate formin-family protein mDia2 as an important mediator of MRTF-stimulated actin polymerization at the leading edge and cell migration. Multiplexed quantitative immunohistochemistry and transcriptome analyses of clinical BC specimens further demonstrate a positive correlation between nuclear localization of MRTF with malignant traits of cancer cells and enrichment of MRTF-SRF gene signature in pair-matched distant metastases versus primary tumors. In conclusion, this study establishes a novel mechanism of MRTF-dependent regulation of cell migration and provides evidence for the association between MRTF activity and increased malignancy in human BC, justifying future development of specific small molecule inhibitors of the MRTF-SRF transcriptional complex as potential therapeutic agents in BC.
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