ArticleMolecular and cellular biology2010
mDia1 targets v-Src to the cell periphery and facilitates cell transformation, tumorigenesis, and invasion.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Role of Nrf2, STAT3, and Src as Molecular Targets for Cancer Chemoprevention.Pharmaceutics · 2022Review
- A Tale of Two States: Normal and Transformed, With and Without Rigidity Sensing.Annual review of cell and developmental biology · 2019Review
- Transactivation of RAGE mediates angiotensin-induced inflammation and atherogenesis.The Journal of clinical investigation · 2019Article
- Enteropathogenic E. coli relies on collaboration between the formin mDia1 and the Arp2/3 complex for actin pedestal biogenesis and maintenance.PLoS pathogens · 2018Article
- Spatial cycles mediated by UNC119 solubilisation maintain Src family kinases plasma membrane localisation.Nature communications · 2017Article
- mDia1 regulates breast cancer invasion by controlling membrane type 1-matrix metalloproteinase localization.Oncotarget · 2016Article
- Multitarget super-resolution microscopy with high-density labeling by exchangeable probes.Nature methods · 2015Article
- Drosophila homologue of Diaphanous 1 (DIAPH1) controls the metastatic potential of colon cancer cells by regulating microtubule-dependent adhesion.Oncotarget · 2015Article
- Endocytosis and the Src family of non-receptor tyrosine kinases.Biomolecular concepts · 2014Review
- Regulation of Src trafficking and activation by the endocytic regulatory proteins MICAL-L1 and EHD1.Journal of cell science · 2014Article
- Rho GTPases modulate malignant transformation of tumor cells.Small GTPases · 2014Review
- Roles of rho GTPases in intracellular transport and cellular transformation.International journal of molecular sciences · 2013Review
- Fibroblast growth factor 2 causes G2/M cell cycle arrest in ras-driven tumor cells through a Src-dependent pathway.PloS one · 2013Article
- Formin mDia1 mediates vascular remodeling via integration of oxidative and signal transduction pathways.Circulation research · 2012Article
- Nucleating actin for invasion.Nature reviews. Cancer · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The small GTPase Rho regulates cell morphogenesis through remodeling of the actin cytoskeleton. While Rho is overexpressed in many clinical cancers, the role of Rho signaling in oncogenesis remains unknown. mDia1 is a Rho effector producing straight actin filaments. Here we transduced mouse embryonic fibroblasts from mDia1-deficient mice with temperature-sensitive v-Src and examined the involvement and mechanism of the Rho-mDia1 pathway in Src-induced oncogenesis. We showed that in v-Src-transduced mDia1-deficient cells, formation of actin filaments is suppressed, and v-Src in the perinuclear region does not move to focal adhesions upon a temperature shift. Consequently, membrane translocation of v-Src, v-Src-induced morphological transformation, and podosome formation are all suppressed in mDia1-deficient cells with impaired tyrosine phosphorylation. mDia1-deficient cells show reduced transformation in vitro as examined by focus formation and colony formation in soft agar and exhibit suppressed tumorigenesis and invasion when implanted in nude mice in vivo. Given overexpression of c-Src in various cancers, these findings suggest that Rho-mDia1 signaling facilitates malignant transformation and invasion by manipulating the actin cytoskeleton and targeting Src to the cell periphery.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.