ArticleProceedings of the National Academy of Sciences of the United States of America1992
Cyclic AMP induces transforming growth factor beta 2 gene expression and growth arrest in the human androgen-independent prostate carcinoma cell line PC-3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 70 citations in OpenAlex.
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- Advances and Challenges in Targeting TGF-β Isoforms for Therapeutic Intervention of Cancer: A Mechanism-Based Perspective.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Orphan nuclear receptor ERRγ regulates hepatic TGF-β2 expression and fibrogenic response in CClArchives of toxicology · 2021Article
- Cellular and Molecular Responses to Mechanical Expansion of Tissue.Frontiers in physiology · 2016Review
- Phosphodiesterase 4D inhibitors limit prostate cancer growth potential.Molecular cancer research : MCR · 2015Article
- Role of phosphodiesterase 2 in growth and invasion of human malignant melanoma cells.Cellular signalling · 2014Article
- Genomic and functional characterizations of phosphodiesterase subtype 4D in human cancers.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Epac inhibits migration and proliferation of human prostate carcinoma cells.British journal of cancer · 2009Article
- Identification of PDE4D as a proliferation promoting factor in prostate cancer using a Sleeping Beauty transposon-based somatic mutagenesis screen.Cancer research · 2009Article
- Suppressor of cytokine signaling-3 antagonizes cAMP effects on proliferation and apoptosis and is expressed in human prostate cancer.The American journal of pathology · 2006Article
- Antitumorigenic actions of growth hormone-releasing hormone antagonists.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Article
- Prostate cancer progression. Implications of histopathology.The American journal of pathology · 1994Review
- Terminal neuroendocrine differentiation of human prostate carcinoma cells in response to increased intracellular cyclic AMP.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
- Growth factors and their receptors as determinants in the proliferation and metastasis of human prostate cancer.Cancer metastasis reviews · 1993Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The standard therapy for advanced prostate cancer is androgen ablation. Despite transitory responses, hormonally treated patients ultimately relapse with androgen-independent disease that is resistant to further hormonal manipulation and cytotoxic chemotherapy. To develop an additional approach to the treatment of advanced prostate cancer, we have been studying the signal transductions controlling the growth of human androgen-independent prostate carcinoma cell lines. We report here that elevation of intracellular cAMP markedly inhibits the growth of the hormone-refractory cell line PC-3. To examine the mechanism of cAMP action in PC-3 cells, we tested the effect of the cAMP analog dibutyryl cAMP (Bt2-cAMP) on the regulation of the potent negative growth factor transforming growth factor beta (TGF-beta). Bt2-cAMP selectively induced the secretion of TGF-beta 2 and not TGF-beta 1 by PC-3 cells. This TGF-beta 2 was shown to be bioactive by using the CCL-64 mink lung cell assay. TGF-beta 1 was not activated despite being present at 3-fold higher concentrations than TGF-beta 2. Northern analysis showed that Bt2-cAMP induced an increase in the five characteristic TGF-beta 2 transcripts and had no effect on the level of TGF-beta 1 or TGF-beta 3 transcripts. TGF-beta 2 induction was only weakly enhanced by cycloheximide and was completely inhibited by actinomycin D. These data show that Bt2-cAMP induces the expression of active TGF-beta 2 by PC-3 prostate carcinoma cells, suggesting a new approach to the treatment of prostate cancer and a new molecular mechanism of cAMP action.
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