ArticleCancer chemotherapy and pharmacology1992
Posttranscriptional regulation of c-myc proto-oncogene expression and growth inhibition by recombinant human interferon-beta ser17 in a human colon carcinoma cell line.
Article in Cancer chemotherapy and pharmacology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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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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.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- SRSF1 acts as an IFN-I-regulated cellular dependency factor decisively affecting HIV-1 post-integration steps.Frontiers in immunology · 2022Article
- The relation between c-myc expression and interferon sensitivity in uveal melanoma.The British journal of ophthalmology · 2004Article
- The 2-5A system: modulation of viral and cellular processes through acceleration of RNA degradation.Pharmacology & therapeutics · 1998Review
- In vivo generation of 3' and 5' truncated species in the process of c-myc mRNA decay.Nucleic acids research · 1996Article
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Recombinant human interferon-beta ser17 (IFN-beta ser17), a cytokine that exhibits both antiviral and antiproliferative activity against a wide variety of cell types, causes a time- and dose-dependent inhibition of monolayer growth and of the expression of the c-myc proto-oncogene in DLD-1 Clone A human colon-carcinoma cells. The suppression of c-myc expression mediated by IFN-beta ser17 is due to a posttranscriptional destabilization of c-myc mRNA rather than to an inhibition of c-myc mRNA transcription. There is evidence suggesting that the selective reduction in the half-life of c-myc mRNA in IFN-beta ser17-treated cells occurs through an increase in the activity of the 2',5'-oligoadenylate synthetase/RNase L [2',5'-oligo (A) synthetase] pathway in DLD-1 Clone A cells. Cotreatment of these cells with IFN-beta ser17 and the anticancer agent N-methylformamide leads to the partial abrogation of 2',5'-oligo (A) synthetase activity and the stabilization of c-myc mRNA. These findings suggest that there is a correlation between the IFN-beta ser17-mediated suppression of c-myc expression and the induction of 2',5'-oligo (A) synthetase activity in DLD-1 clone A cells.
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Registered trials
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