ArticleCancer cell & microenvironment
Role of caveolin-2 in subcutaneous tumor growth and angiogenesis associated with syngeneic mouse Lewis lung carcinoma and B16 melanoma models.
Article in Cancer cell & microenvironment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 3 citations in OpenAlex.
- Therapeutic role of caveolin family in stem cell fate and development for management of chronic degenerative diseases: A scientometric study to an in-depth review.Journal of advanced research · 2026Review
- Tracking cellular and molecular changes in a species-specific manner during experimental tumor progressionOncotarget · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In addition to cancer cells, primary tumors are composed of a multitude of stromal cell types. Among others, the stromal cell types involved in tumor growth and progression include endothelial cells, fibroblasts, pericytes, stem cells and various cell types of immune origin. While the role of oncogenes or tumor suppressor proteins expressed in cancer cells has been extensively studied, far less is known about potential involvement of proteins expressed in stromal cell types present within the tumor microenvironment. Recent experimental evidence from our laboratory suggests that caveolin-2 (Cav-2) protein expressed in stromal cell types of the tumor microenvironment promotes subcutaneous tumor growth in two independent syngeneic mouse models, i.e., Lewis lung carcinoma (LLC) and B16-F10 melanoma. Mechanistically, the tumor growth promoting role of Cav-2 is associated with enhanced tumor induced neovascularization. At the molecular level, host-expressed Cav-2 appears to prevent excessive expression of anti-angiogenic thrombospondin-1 (TSP-1) and promote phosphorylation of pro-angiogenic endothelial nitric oxide synthase (eNOS) at serine 1177. Taken together, our recent findings suggest that Cav-2 expressed within the tumor microenvironment could be a potential target for anti-cancer therapy.
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Registered trials
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