ArticleThe Journal of cell biology1996
Treatment of melanoma cells with the synthetic retinoid CD437 induces apoptosis via activation of AP-1 in vitro, and causes growth inhibition in xenografts in vivo.
Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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Who cites it
19 citing papers in PubMed, 105 citations in OpenAlex.
- Bactericidal and Anti-biofilm Activity of the Retinoid Compound CD437 AgainstFrontiers in microbiology · 2019Article
- Article
- The antitumor toxin CD437 is a direct inhibitor of DNA polymerase α.Nature chemical biology · 2016Article
- Nuclear receptor 4A (NR4A) family - orphans no more.The Journal of steroid biochemistry and molecular biology · 2016Article
- Minireview: role of orphan nuclear receptors in cancer and potential as drug targets.Molecular endocrinology (Baltimore, Md.) · 2014Review
- The lipophilic bullet hits the targets: medicinal chemistry of adamantane derivatives.Chemical reviews · 2013Review
- Adamantyl-substituted retinoid-related molecules induce apoptosis in human acute myelogenous leukemia cells.Molecular cancer therapeutics · 2010Article
- Chemoresistance acquisition induces a global shift of expression of aniogenesis-associated genes and increased pro-angogenic activity in neuroblastoma cells.Molecular cancer · 2009Article
- Involvement of thioredoxin-binding protein 2 in the antitumor activity of CD437.Cancer science · 2008Article
- C-Fos expression is a molecular predictor of progression and survival in epithelial ovarian carcinoma.British journal of cancer · 2008Article
- Adamantyl-substituted retinoid-related molecules bind small heterodimer partner and modulate the Sin3A repressor.Cancer research · 2007Article
- Mitochondriotoxic compounds for cancer therapy.Oncogene · 2006Review
- Early events in the induction of apoptosis in ovarian carcinoma cells by CD437: activation of the p38 MAP kinase signal pathway.Oncogene · 2003Article
- Review
- Implication of multiple mechanisms in apoptosis induced by the synthetic retinoid CD437 in human prostate carcinoma cells.Oncogene · 2000Article
- Implication of c-Myc in apoptosis induced by the retinoid CD437 in human lung carcinoma cells.Oncogene · 1999Article
- Mechanisms of apoptosis induced by the synthetic retinoid CD437 in human non-small cell lung carcinoma cells.Oncogene · 1999Article
- Retinoids: present role and future potential.British journal of cancer · 1999Review
- Molecular determinants of AHPN (CD437)-induced growth arrest and apoptosis in human lung cancer cell lines.Molecular and cellular biology · 1998Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human malignant melanoma is notoriously resistant to pharmacological modulation. We describe here for the first time that the synthetic retinoid CD437 has a strong dose-dependent antiproliferative effect on human melanoma cells (IC50: 5 x 10(-6) M) via the induction of programmed cell death, as judged by analysis of cell morphology, electron microscopical features, and DNA fragmentation. Programmed cell death was preceded by a strong activation of the AP-1 complex in CD437-treated cells as demonstrated by gel retardation and chloramphenicol transferase (CAT) assays. Northern blot analysis showed a time-dependent increase in the expression of c-fos and c-jun encoding components of AP-1, whereas bcl-2 and p53 mRNA levels remained constant. CD437 also exhibited a strong growth inhibitory effect on MeWo melanoma cells in a xenograft model. In tissue sections of CD437-treated MeWo tumors from these animals, apoptotic melanoma cells and c-fos overexpressing cells were colocalized by TdT-mediated deoxyuridine triphosphate-digoxigenin nick end labeling (TUNEL) staining and in situ hybridization. Taken together, this report identifies CD437 as a retinoid that activates and upregulates the transcription factor AP-1, leading eventually to programmed cell death of exposed human melanoma cells in vitro and in vivo. Further studies are needed to evaluate whether synthetic retinoids such as CD437 represent a new class of retinoids, which may open up new ways to a more effective therapy of malignant melanoma.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.