MicroRNA-200c Represses Migration and Invasion of Breast Cancer Cells by Targeting Actin-Regulatory Proteins FHOD1 and PPM1F

Jurmeister, Sarah; Baumann, Marek; Balwierz, Aleksandra; Keklikoglou, Ioanna; Ward, Adrian; Uhlmann, Stefan; Zhang, Jitao David; Wiemann, Stefan; Şahin, Özgür

doi:10.1128/mcb.06212-11

Cited by 214 publications

(197 citation statements)

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“…Up-regulated miR-21, miR-222 and miR-29a were associated with the chemoresistance of breast cancer MCF-7/ADR cells to ADR through direct interaction with anti-apoptotic protein PTEN (Wang et al, 2011;Zhong et al, 2013). Down-regulated miR-34a and miR-200 modulates chemosensitivity of breast cancer cells to adriamycin by targeting Notch1 and E-cadherin, respectively, which regulated the formation of cancer stem cells (CSCs) and contributed to the acquisition of the epithelialemesenchymal transition (EMT) phenotype (Tryndyak et al, 2010;Howe et al, 2011;Jurmeister et al, 2012;Li et al, 2012). Accordingly, it is quite necessary to understand the functions of miRNAs in the process of drug resistance in the hope of overcoming drug resistance through modulating miRNA regulation.…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of miRNA-452 is Associated with Adriamycin-resistance in Breast Cancer Cells

Gong²,

Li³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 99%

Down-regulation of miRNA-452 is Associated with Adriamycin-resistance in Breast Cancer Cells

Gong²,

Li³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Another common feature of formins consists of their ability to induce the nuclear transcription serum response factor (SRF) to modulate the expression of specific target genes (Tominaga et al, 2000). This effect mirrors formin-mediated regulation of actin dynamics since enhanced actin polymerization liberates myocardin-related transcription factor (MRTF) cofactors from G-actin to facilitate their import into the nucleus and subsequent activation of transcription (Jurmeister et al, 2012;Staus et al, 2011). As activated FHOD1 acts as potent inducer of SRF-mediated transcription (Gasteier et al, 2003;Westendorf, 2001) without inducing de novo actin polymerization, our results indicate that reducing G-actin pools, e.g.…”

Section: Fhod1 Bundling In Actin Arcs 1897mentioning

confidence: 99%

FHOD1 is a combined actin filament capping and bundling factor that selectively associates with actin arcs and stress fibers

Schönichen

Mannherz

Behrmann

et al. 2013

Journal of Cell Science

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SummaryFormins are actin polymerization factors that are known to nucleate and elongate actin filaments at the barbed end. In the present study we show that human FHOD1 lacks actin nucleation and elongation capacity, but acts as an actin bundling factor with capping activity toward the filament barbed end. Constitutively active FHOD1 associates with actin filaments in filopodia and lamellipodia at the leading edge, where it moves with the actin retrograde flow. At the base of lamellipodia, FHOD1 is enriched in nascent, bundled actin arcs as well as in more mature stress fibers. This function requires actin-binding domains located N-terminally to the canonical FH1-FH2 element. The bundling phenotype is maintained in the presence of tropomyosin, confirmed by electron microscopy showing assembly of 5 to 10 actin filaments into parallel, closely spaced filament bundles. Taken together, our data suggest a model in which FHOD1 stabilizes actin filaments by protecting barbed ends from depolymerization with its dimeric FH2 domain, whereas the region N-terminal to the FH1 domain mediates F-actin bundling by simultaneously binding to the sides of adjacent F-actin filaments.

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“…At present, >1000 miRs have been identified in the human and mouse genomes, a number of which have been found to be involved in cell migration (4,5). It has been reported that miRs, including miR-let-7a, -16, -30a, -34a, -107, -125b, -200c, -203, -218, -424 and -488, inhibit the migration of specific tumor cells and other normal cell lineages (5)(6)(7)(8)(9)(10)(11)(12)(13)(14). However, other miRs, including miR-10b, -20, -21 and -144, have been reported to promote cell migration (15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

microRNA-10b promotes the migration of mouse bone marrow-derived mesenchymal stem cells and downregulates the expression of E-cadherin

Zhang

Jing

Ren

et al. 2013

Molecular Medicine Reports

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Abstract. The ability of mesenchymal stem cells (MSCs) to migrate is an important determinant of the efficiency of MSC transplant therapy. MicroRNA-10b (miR-10b) has been positively involved in the migration of a number of tumor cells lineages. To date, it remains unknown whether miR-10b affects the migration of MSCs. In the current study, the effect of miR-10b on the migration of mouse bone marrowderived MSCs (bmMSCs) was investigated. Third-passage bmMSCs were transfected with miR-10b mimic and negative control precursor miRNA using Lipofectamine™ 2000. miR-10b and E-cadherin expression and bmMSC migration were determined. The present results showed that primary bmMSCs exhibit a spindled or triangular morphology and that third-passage bmMSCs present a typical fibroblast-like morphology, exhibiting CD90-positive and CD45-negative expression. Compared with the transfection of negative control miRNA, transfection of miR-10b mimic markedly upregulated miR-10b expression in bmMSCs, increased their migration and downregulated E-cadherin expression. The current observations indicate that the upregulation of miR-10b increases bmMSC migration ability, which may be involved in the downregulation of E-cadherin. IntroductionMesenchymal stem cells (MSCs) are multipotent cells that may differentiate into a variety of cell lineages, including osteocytes, adipocytes, chondrocytes, endothelial cells, cardiomyocytes and neurons, when exposed to appropriate conditions (1,2). Bone marrow-derived MSCs (bmMSCs) are a commonly used source of stem cells. To date, bmMSCs have been widely applied in tissue engineering. The migration capability of bmMSCs is an important determinant of the efficiency of bmMSC-based transplant therapy. A previous study showed that ~1.5% of injected stem cells reached the injured tissue following intracoronary injection for 2 h (3). However, the low homing rate of bmMSCs severely limits their clinical uses.MicroRNAs (miRs) are endogenous, small, noncoding RNAs in eukaryotic cells (4). miRs are post-transcriptional regulators that negatively regulate gene expression by binding to the target mRNA for degradation and translational repression (4). At present, >1000 miRs have been identified in the human and mouse genomes, a number of which have been found to be involved in cell migration (4,5). It has been reported that miRs, including miR-let-7a, -16, -30a, -34a, -107, -125b, -200c, -203, -218, -424 and -488, inhibit the migration of specific tumor cells and other normal cell lineages (5-14). However, other miRs, including miR-10b, -20, -21 and -144, have been reported to promote cell migration (15)(16)(17)(18).To date, the effects of miR-10b on the migration and invasion of tumor cells have been well studied (15,19,20). However, little is known about the function of miR-10b in the migration of bmMSCs. In the present study, the role of miR-10b in bmMSC migration and E-cadherin expression was investigated. Materials and methodsIsolation and culture of bmMSCs. bmMSCs were isolated and cultured as previously de...

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MicroRNA-200c Represses Migration and Invasion of Breast Cancer Cells by Targeting Actin-Regulatory Proteins FHOD1 and PPM1F

Cited by 214 publications

References 50 publications

Down-regulation of miRNA-452 is Associated with Adriamycin-resistance in Breast Cancer Cells

Down-regulation of miRNA-452 is Associated with Adriamycin-resistance in Breast Cancer Cells

FHOD1 is a combined actin filament capping and bundling factor that selectively associates with actin arcs and stress fibers

microRNA-10b promotes the migration of mouse bone marrow-derived mesenchymal stem cells and downregulates the expression of E-cadherin

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