ArticleCancer research2006
Activation of Vav/Rho GTPase signaling by CXCL12 controls membrane-type matrix metalloproteinase-dependent melanoma cell invasion.
Article in Cancer research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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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.
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Who cites it
64 citing papers in PubMed, 125 citations in OpenAlex.
- Invadopodia in cancer metastasis: dynamics, regulation, and targeted therapies.Journal of translational medicine · 2025Review
- Stromal Expression Profiling Reveals Immune-Driven Adaption to Malignancy in Canine Melanoma Subtypes.Veterinary and comparative oncology · 2025Article
- CD169iScience · 2024Article
- TIAM-1 regulates polarized protrusions during dorsal intercalation in the Caenorhabditis elegans embryo through both its GEF and N-terminal domains.Journal of cell science · 2024Article
- The scaffold RhoGAP protein ARHGAP8/BPGAP1 synchronizes Rac and Rho signaling to facilitate cell migration.Molecular biology of the cell · 2023Article
- CXCL12/CXCR4-Rac1-mediated migration of osteogenic precursor cells contributes to pathological new bone formation in ankylosing spondylitis.Science advances · 2022Article
- GPCRs thatSmall GTPases · 2022Review
- Vav1 Sustains the In Vitro Differentiation of Normal and Tumor Precursors to Insulin Producing Cells Induced by all-Trans Retinoic Acid (ATRA).Stem cell reviews and reports · 2021Article
- Targeting Rac and Cdc42 GEFs in Metastatic Cancer.Frontiers in cell and developmental biology · 2020Review
- Interleukin-6 promotes pancreatic cancer cell migration by rapidly activating the small GTPase CDC42.The Journal of biological chemistry · 2018Article
- Vav1 downmodulates Akt in different breast cancer subtypes: a new promising chance to improve breast cancer outcome.Molecular oncology · 2018Article
- Total alkaloids ofOncology letters · 2018Article
- Elevated level of Vav1 was correlated with advanced biological behavior and poor prognosis in patients with gastric cancer.International journal of clinical and experimental pathology · 2018Article
- Chaperone-mediated autophagy substrate proteins in cancer.Oncotarget · 2017Review
- Phosphorylated cortactin recruits Vav2 guanine nucleotide exchange factor to activate Rac3 and promote invadopodial function in invasive breast cancer cells.Molecular biology of the cell · 2017Article
- Multi-factorial modulation of colorectal carcinoma cells motility - partial coordination by the tetraspanin Co-029/tspan8.Oncotarget · 2017Article
- Review
- MST3 promotes proliferation and tumorigenicity through the VAV2/Rac1 signal axis in breast cancer.Oncotarget · 2016Article
- BMI1 induces an invasive signature in melanoma that promotes metastasis and chemoresistance.Genes & development · 2016Article
- Vav1: A Dr. Jekyll and Mr. Hyde protein--good for the hematopoietic system, bad for cancer.Oncotarget · 2015Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Melanoma cells express the chemokine receptor CXCR4, which confers invasive signals on binding to its ligand CXCL12. We show here that knocking down membrane-type matrix metalloproteinase (MT1-MMP) expression translates into a blockade of invasion across reconstituted basement membranes and type I collagen gels in response to CXCL12, which is the result of lack of MMP-2 activation. Interference with MMP-2 expression further confirms its important role during this invasion. Vav proteins are guanine-nucleotide exchange factors for Rho GTPases that regulate actin dynamics and gene expression. We show that melanoma cells express Vav1 and Vav2, which are activated by CXCL12 involving Jak activity. Blocking Vav expression by RNA interference results in impaired activation of Rac and Rho by CXCL12 and in a remarkable inhibition of CXCL12-promoted invasion. Importantly, up-regulation of MT1-MMP expression by CXCL12, a mechanism contributing to melanoma cell invasion, is blocked by knocking down Vav expression or by inhibiting Jak. Together, these data indicate that activation of Jak/Vav/Rho GTPase pathway by CXCL12 is a key signaling event for MT1-MMP/MMP-2-dependent melanoma cell invasion.
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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.