ArticleMarine drugs2014
Chromomycin A2 induces autophagy in melanoma cells.
Article in Marine drugs, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
The trial behind it
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
14 citing papers in PubMed, 23 citations in OpenAlex.
- Anticancer Potential of Piericidin A1 and Derivatives Isolated From Streptomyces sp. Associated With Palythoa variabilis From Brazilian Reefs.Chemistry & biodiversity · 2026Article
- Antibacterial, Antifungal, and Cytotoxic Effects of EndophyticBiomedicines · 2024Article
- Article
- Natural Products from Singapore Soil-DerivedMolecules (Basel, Switzerland) · 2023Article
- Chromomycin AFrontiers in immunology · 2022Article
- Chromomycin A3 suppresses cholangiocarcinoma growth by induction of S phase cell cycle arrest and suppression of Sp1‑related anti‑apoptotic proteins.International journal of molecular medicine · 2020Article
- From Seabed to Bedside: A Review on Promising Marine Anticancer Compounds.Biomolecules · 2020Review
- Targeting the Oncogenic TBX2 Transcription Factor With Chromomycins.Frontiers in chemistry · 2020Article
- Bacteria in Cancer Therapeutics: A Framework for Effective Therapeutic Bacterial Screening and Identification.Journal of Cancer · 2019Review
- Chromomycin AThe Journal of general physiology · 2018Article
- Identification of gene expression levels in primary melanoma associated with clinically meaningful characteristics.Melanoma research · 2018Article
- Marine drugs for cancer: surfacing biotechnological innovations from the oceans.Clinics (Sao Paulo, Brazil) · 2018Review
- Tumor Protein (TP)-p53 Members as Regulators of Autophagy in Tumor Cells upon Marine Drug Exposure.Marine drugs · 2016Article
- Blue-Print Autophagy: Potential for Cancer Treatment.Marine drugs · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study highlights the biological effects of chromomycin A2 toward metastatic melanoma cells in culture. Besides chromomycin A2, chromomycin A3 and demethylchromomycin A2 were also identified from the extract derived from Streptomyces sp., recovered from Paracuru Beach, located in the northeast region of Brazil. The cytotoxic activity of chromomycin A2 was evaluated across a panel of human tumor cell lines, which found IC50 values in the nM-range for exposures of 48 and 72 h. MALME-3M, a metastatic melanoma cell line, showed the highest sensitivity to chromomycin A2 after 48h incubation, and was chosen as a model to investigate this potent cytotoxic effect. Treatment with chromomycin A2 at 30 nM reduced cell proliferation, but had no significant effect upon cell viability. Additionally, chromomycin A2 induced accumulation of cells in G0/G1 phase of the cell cycle, with consequent reduction of S and G2/M and unbalanced expression of cyclins. Chromomycin A2 treated cells depicted several cellular fragments resembling autophagosomes and increased expression of proteins LC3-A and LC3-B. Moreover, exposure to chromomycin A2 also induced the appearance of acidic vacuolar organelles in treated cells. These features combined are suggestive of the induction of autophagy promoted by chromomycin A2, a feature not previously described for chromomycins.
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Registered trials
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.