ArticleOncotarget2014
Vav1 promotes lung cancer growth by instigating tumor-microenvironment cross-talk via growth factor secretion.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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
12 citing papers in PubMed, 16 citations in OpenAlex.
- Transcriptome and Metabolome Analyses Reveal the Mechanism of Corpus Luteum Cyst Formation in Pigs.Genes · 2023Article
- Review
- Nanoparticles overcome adaptive immune resistance and enhance immunotherapyFrontiers in pharmacology · 2023Review
- Soluble HLA peptidome of pleural effusions is a valuable source for tumor antigens.Journal for immunotherapy of cancer · 2022Article
- Vav1 Promotes B-Cell Lymphoma Development.Cells · 2022Article
- Vav1 and mutant K-Ras synergize in the early development of pancreatic ductal adenocarcinoma in mice.Life science alliance · 2020Article
- Model-free feature screening for categorical outcomes: Nonlinear effect detection and false discovery rate control.PloS one · 2019Article
- 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
- TGFβ promotes mesenchymal phenotype of pancreatic cancer cells, in part, through epigenetic activation of VAV1.Oncogene · 2017Article
- Vav1: A Dr. Jekyll and Mr. Hyde protein--good for the hematopoietic system, bad for cancer.Oncotarget · 2015Review
- Clinical significance and prognostic value of Vav1 expression in Non-small cell lung cancer.American journal of cancer research · 2015Article
- RhoA G17E/Vav1 Signaling Induces Cancer Invasion via Matrix Metalloproteinase-9 in Gastric Cancer.Technology in cancer research & treatmentArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vav1 is a signal transducer that functions as a scaffold protein and a regulator of cytoskeleton organization in the hematopoietic system, where it is exclusively expressed. Recently, Vav1 was shown to be involved in diverse human cancers, including lung cancer. We demonstrate that lung cancer cells that abnormally express Vav1 secrete growth factors in a Vav1-dependent manner. Transcriptome analysis demonstrated that Vav1 depletion results in a marked reduction in the expression of colony-stimulating-factor-1 (CSF1), a hematopoietic growth factor. The association between Vav1 expression and CSF1 was further supported by signal transduction experiments, supporting involvement of Vav1 in regulating lung cancer secretome. Blocking of ERK phosphorylation, led to a decrease in CSF1 transcription, thus suggesting a role for ERK, a downstream effector of Vav1, in CSF1 expression. CSF1-silenced cells exhibited reduced focus formation, proliferation abilities, and growth in NOD/SCID mice. CSF1-silenced H358 cells resulted in significantly smaller tumors, showing increased fibrosis and a decrease in tumor infiltrating macrophages. Finally, immunohistochemical analysis of primary human lung tumors revealed a positive correlation between Vav1 and CSF1 expression, which was associated with tumor grade. Additional results presented herein suggest a potential cross-talk between cancer cells and the microenvironment controlled by CSF1/Vav1 signaling pathways.
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Registered trials
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