MicroRNA control of podosome formation in vascular smooth muscle cells in vivo and in vitro

Quintavalle, Manuela; Elia, Leonardo; Condorelli, Gianluigi; Courtneidge, Sara A.

doi:10.1083/jcb.200912096

Cited by 188 publications

(171 citation statements)

References 44 publications

Supporting

Mentioning

159

Contrasting

Unclassified

Order By: Relevance

“…Similarly, fascin-depletion altered colon carcinoma cell protrusion morphology, and decreased (i) the numbers of filopodia, (ii) Rac-dependent migration on laminin, (iii) turnover of focal adhesions and (iv) tumor development and metastasis in vivo (Hashimoto et al, 2007). In accordance with the cytoskeletal restructuring demonstrated by our study, miR-145-dependent regulation of fascin expression was suggested to modulate podosome formation in vascular smooth muscle cells (Quintavalle et al, 2010), with implications for the regulation of cell motility.…”

Section: Jam-a Is a Direct Target Of Transcriptional Regulation By MIsupporting

confidence: 69%

“…In addition to JAM-A, miR-145-dependent regulation of fascin may have contributed to the migratory phenotype. Fascin bundles lamellopodial actin filaments into filopodia (Hashimoto et al, 2007), and is a direct target of miR-145 in bladder cancer, esophageal squamous cell carcinoma and 3T3 cells (Chiyomaru et al, 2010;Kano et al, 2010;Quintavalle et al, 2010). Increased fascin expression enhances, and decreased expression reduces cell motility in esophageal squamous cell, gastric, prostate and colorectal cancer (Vignjevic et al, 2007;Darnel et al, 2009;Kim et al, 2009b;Qualtrough et al, 2009;Kano et al, 2010), and correlates with metastasis (Darnel et al, 2009).…”

Section: Jam-a Is a Direct Target Of Transcriptional Regulation By MImentioning

confidence: 99%

See 1 more Smart Citation

miR-145-dependent targeting of Junctional Adhesion Molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness

et al. 2010

View full text Add to dashboard Cite

Micro RNAs are small non-coding RNAs, which regulate fundamental cellular and developmental processes at the transcriptional and translational level. In breast cancer, miR-145 expression is downregulated compared with healthy control tissue. As several predicted targets of miR-145 potentially regulate cell motility, we aimed at investigating a potential role for miR-145 in breast cancer cell motility and invasiveness. Assisted by Affymetrix array technology, we demonstrate that overexpression of miR-145 in MDA-MB-231, MCF-7, MDA-MB-468 and SK-BR-3 breast cancer cells and in Ishikawa endometrial carcinoma cells leads to a downregulation of the cell-cell adhesion protein JAM-A and of the actin bundling protein fascin. Moreover, podocalyxin and Serpin E1 mRNA levels were downregulated, and gamma-actin, transgelin and MYL9 were upregulated upon miR-145 overexpression. These miR-145-dependent expression changes drastically decreased cancer cell motility, as revealed by time-lapse video microscopy, scratch wound closure assays and matrigel invasion assays. Immunofluorescence microscopy demonstrated restructuring of the actin cytoskeleton and a change in cell morphology by miR-145 overexpression, resulting in a more cortical actin distribution, and reduced actin stress fiber and filopodia formation. Nuclear rotation was observed in 10% of the pre-miR-145 transfected MDA-MB-231 cells, accompanied by a reduction of perinuclear actin. Luciferase activation assays confirmed direct miR-145-dependent regulation of the 3 0 UTR of JAM-A, whereas siRNA-mediated knockdown of JAM-A expression resulted in decreased motility and invasiveness of MDA-MB-231 and MCF-7 breast cancer cells. Our data identify JAM-A and fascin as novel targets of miR-145, firmly establishing a role for miR-145 in modulating breast cancer cell motility. Our data provide a rationale for future miR-145-targeted approaches of antimetastatic cancer therapy.

show abstract

Section: Jam-a Is a Direct Target Of Transcriptional Regulation By MIsupporting

confidence: 69%

Section: Jam-a Is a Direct Target Of Transcriptional Regulation By MImentioning

confidence: 99%

miR-145-dependent targeting of Junctional Adhesion Molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness

et al. 2010

View full text Add to dashboard Cite

show abstract

“…28,[30][31][32][33] Collectively, these findings indicate that fascin-1 functionally The molecular mechanisms of transcriptional regulation of fascin-1 have not been fully elucidated; however, the cAMP response elementbinding protein and aryl hydrocarbon receptor are candidate-positive regulators that enhance the promoter activity of fascin-1. 23,34 In contrast, several miRNAs, such as miR-133a, 133b, 143 and 145, are thought to negatively regulate the fascin-1 transcript in vascular smooth muscle cells 35 and carcinoma cells including urothelial carcinoma cells and squamous cell carcinoma cells. 18,36 These miRNAs have conserved sequences in the 3 0 untranslated region of fascin-1.…”

Section: Discussionmentioning

confidence: 99%

Fascin-1 overexpression and miR-133b downregulation in the progression of gastrointestinal stromal tumor

2013

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are small, non-coding RNAs that are up-or downregulated in several types of cancer, and have an important role in the tumorigenesis and progression. To better understand the role of aberrantly expressed miRNAs and their target genes affecting the biology of gastrointestinal stromal tumor (GIST), we performed miRNA array in 19 cases of GIST, and found that several miRNAs, including miR-133b, were downregulated in high-grade GISTs. Subsequently, quantitative real-time reverse transcription-PCR revealed that fascin-1 mRNA was upregulated in accordance with miR-133b downregulation in high-grade GIST; this result was consistent with a previous report showing that fascin-1 might be a direct target of miR-133b. We then examined the fascin-1 protein expression by immunohistochemical staining in 147 cases of GIST, and found that fascin-1 overexpression was significantly correlated with shorter disease-free survival time and several aggressive pathological factors, including tumor size, mitotic counts, risk grade, blood vessel invasion and mucosal ulceration. Our results suggest that downregulation of miR-133b and overexpression of fascin-1 may have an important role in the progression of GIST, and that fascin-1 may be a useful biomarker to predict the aggressive behavior.

show abstract

“…An increasing amount of experimental evidence has strongly supported that miRNAs are a critical regulator in controlling processes that underlie cell proliferation, differentiation and apoptosis in diverse organisms during normal development (Hassan et al 2012;Zhang et al 2013;Yang et al 2014). MiR-143, which was originally detected during adipocyte differentiation (Esau et al 2004), in many studies has emerged as an essential regulator of cellular physiology, particularly in tumorigenesis and cancer (Akao et al 2009;Quintavalle et al 2010;Qian et al 2013). In addition, recent studies show that miR-143 regulates the vascular smooth muscle cell phenotype (Boucher et al 2011).…”

Section: Discussionmentioning

confidence: 99%

miR-143 inhibits proliferation and induces apoptosis of mammary epithelial cells in dairy goat

Wang

Hou

et al. 2016

Animal Cells and Systems

View full text Add to dashboard Cite

MicroRNAs are a class of post-transcriptional regulators of gene expression in multicellular organisms, which play important roles in cell fate, organ morphogenesis and carcinogenesis. In the present study, we demonstrated the critical roles of miR-143 on mammary epithelial cells of dairy goat. The test results of cell count, methylthiazolyldiphenyl-tetrazolium bromide, Hoechst33342/PI (propidium iodide) and flow cytometry showed miR-143-induced G0/G1 phase arrest, inhibited proliferation and promoted apoptosis of mammary epithelial cells; the qRT-PCR test of marker genes related to cell proliferation and apoptosis, BAX and BCL-2, supported the same conclusions. Our study presents evidence that miR-143 is an important post-transcription regulator involving in mammary cells survival, and it may have a value function in mammary gland development, lactation or involution.ARTICLE HISTORY

show abstract

MicroRNA control of podosome formation in vascular smooth muscle cells in vivo and in vitro

Abstract: PDGF enhances podosome formation and cell migration by regulating expression of the microRNAs miR-143 and -145, which target PDGF-R, PKC-ε, and fascin.

Cited by 188 publications

References 44 publications

miR-145-dependent targeting of Junctional Adhesion Molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness

miR-145-dependent targeting of Junctional Adhesion Molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness

Fascin-1 overexpression and miR-133b downregulation in the progression of gastrointestinal stromal tumor

miR-143 inhibits proliferation and induces apoptosis of mammary epithelial cells in dairy goat

Contact Info

Product

Resources

About