ArticleCancer cell international2007
Caveolin-1 sensitizes rat pituitary adenoma GH3 cells to bromocriptine induced apoptosis.
Article in Cancer cell international, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 58 citations in OpenAlex.
- Association of Mental Health-Related Proteins DAXX, DRD3, and DISC1 With the Progression and Prognosis of Chondrosarcoma.Frontiers in molecular biosciences · 2019Article
- Neurotransmitter receptors as signaling platforms in anterior pituitary cells.Molecular and cellular endocrinology · 2018Review
- Phosphotyrosine profiling of curcumin-induced signaling.Clinical proteomics · 2016Article
- Caveolin-1 mediates Fas-BID signaling in hyperoxia-induced apoptosis.Free radical biology & medicine · 2011Article
- mTOR inhibition reduces cellular proliferation and sensitizes pituitary adenoma cells to ionizing radiation.Surgical neurology international · 2011Article
- Cholesterol and phytosterols differentially regulate the expression of caveolin 1 and a downstream prostate cell growth-suppressor gene.Cancer epidemiology · 2010Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProlactinoma is the most frequent pituitary tumor in humans. The dopamine D2 receptor agonist bromocriptine has been widely used clinically to treat human breast tumor and prolactinoma through inhibition of hyperprolactinemia and induction of tumor cell apoptosis, respectively, but the molecular mechanism of bromocriptine induction of pituitary tumor apoptosis remains unclear. Caveolin-1 is a membrane-anchored protein enriched on caveolae, inverted flask-shaped invaginations on plasma membranes where signal transduction molecules are concentrated. Currently, caveolin-1 is thought to be a negative regulator of cellular proliferation and an enhancer of apoptosis by blocking signal transduction between cell surface membrane receptors and intracellular signaling protein cascades. Rat pituitary adenoma GH3 cells, which express endogenous caveolin-1, exhibit increased apoptosis and shrinkage after exposure to bromocriptine. Hence, the GH3 cell line is an ideal model for studying the molecular action of bromocriptine on prolactinoma.
resultsThe expression of endogenous caveolin-1 in GH3 cells was elevated after bromocriptine treatment. Transiently expressed mouse recombinant caveolin-1 induced apoptosis in GH3 cells by enhancing the activity of caspase 8. Significantly, caveolin-1 induction of GH3 cell apoptosis was sensitized by the administration of bromocriptine. Phosphorylation of caveolin-1 at tyrosine 14 was enhanced after bromocriptine treatment, suggesting that bromocriptine-induced phosphorylation of caveolin-1 may contribute to sensitization of apoptosis in GH3 cells exposed to bromocriptine.
conclusionOur results reveal that caveolin-1 increases sensitivity for apoptosis induction in pituitary adenoma GH3 cells and may contribute to tumor shrinkage after clinical bromocriptine treatment.
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Registered trials
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