ArticleBritish journal of cancer1996
Genes related to growth and invasiveness are repressed by sodium butyrate in ovarian carcinoma cells.
Article in British journal of cancer, 1996. 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.
- The role of the microbiome in ovarian cancer: mechanistic insights into oncobiosis and to bacterial metabolite signaling.Molecular medicine (Cambridge, Mass.) · 2021Review
- Molecular insights of Gas6/TAM in cancer development and therapy.Cell death & disease · 2017Review
- Fractionation of an Extract of Pluchea odorata Separates a Property Indicative for the Induction of Cell Plasticity from One That Inhibits a Neoplastic Phenotype.Evidence-based complementary and alternative medicine : eCAM · 2012Article
- Butyrate reduces liver metastasis of rat colon carcinoma cells in vivo and resistance to oxidative stress in vitro.Clinical & experimental metastasis · 2004Article
- Sodium butyrate modulates cell cycle-related proteins in HT29 human colonic adenocarcinoma cells.Cell proliferation · 2000Article
- Molecular Events as Targets of Anticancer Drug Therapy.Pathology oncology research : POR · 1997Article
Corrections and comments
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Authors and funding
7 authors.
Funding
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Abstract
Down-regulation of oncogene expression is one of the hallmarks of the process whereby transformed cells are forced into differentiation and/or growth arrest by potent inducers and therefore can represent an interim end point in cancer treatment. The differentiation inducer sodium butyrate (NaB) arrested growth of N.1 ovarian carcinoma cells and repressed expression of cyclin D1/prad1 and the invasiveness-related protease plasminogen activator-urokinase (plau). This was accompanied by the acquisition of a differentiated morphology, all of which characteristics were maintained as long as N.1 cells were exposed to the inducer. In accordance with a differentiated phenotype was the finding that fibronectin expression was increased significantly. Recently, it was shown that NaB represses the transcription factor c-myc by blocking Ca2+ signals and modulating serine threonine kinase activity. We wanted to investigate NaB-mediated interference on signals contributing to the expression on prad1, plau and growth arrest-specific 6 (gas6). Protein kinase A (PKA) inactivation de-repressed prad1 and plau transcript levels. NaB had onlygeneral but no specific influence on PKA-modulated prad1 and plau expression however. Protein kinase C activation up-regulated plau transcript levels, but not that of prad1. Prad1 expression seemed to depend on Ca2+-triggered signals. Constitutive plau expression was insensitive to additional Ca2+-mediated signals, but it became responsive upon NaB treatment.
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