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Ecteinascidin-743 (ET-743), a natural marine compound, with a unique mechanism of action
Abstract
The mode of action of Ecteinascidin-743 (ET-743), a marine tetrahydroisoquinoline alkaloid isolated from Ecteinascidia turbinata, which has shown very potent antitumour activity in preclinical systems and encouraging results in Phase I clinical trials was investigated at a cellular level. Both SW620 and LoVo human intestinal carcinoma cell lines exposed for 1 h to ET-743 progress through S phase more slowly than control cells and then accumulate in the G2M phase. The sensitivity to ET-743 of G1 synchronised cells was much higher than that of cells synchronised in S phase and even higher than that of cells synchronised in G2M. ET-743 concentrations up to four times higher than the IC(50) value caused no detectable DNA breaks or DNA-protein cross-links as assessed by alkaline elution techniques. ET-743 induced a significant increase in p53 levels in cell lines expressing wild-type (wt) (p53). However, the p53 status does not appear to be related to the ET-743 cytotoxic activity as demonstrated by comparing the drug sensitivity in p53 (-/-) or (+/+) mouse embryo fibroblasts and in A2780 ovarian cancer cells or the A2780/CX3 sub-line transfected with a dominant-negative mutant TP53. The cytotoxic potency of ET-743 was comparatively evaluated in CHO cell lines proficient or deficient in nucleotide excision repair (NER), and it was found that ET-743 was approximately 7-8 times less active in ERCC3/XPB and ERCC1-deficient cells than control cells. The findings that G1 phase cells are hypersensitive and that NER-deficient cells are resistant to ET-743 indicate that the mode of action of ET-743 is unique and different from that of other DNA-interacting drugs.
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“Moreover, ET-743, a tetrahydroisoquinilone alkaloid isolated from tunicate Ecteinascidia turbinata entered phase I clinical trials [62], since it exerts anti-proliferative effects by selective alkylation of guanine residues in the DNA minor groove [63], whereas dolastatin 10, a member of a peptide family isolated from the mollusk Dolabella auricularia, reached phase II clinical trials [64], based”
From Marine Natural Products: A Source of Novel Anticancer Drugs (2019) · cites this paper as [63]
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Self-citation
Metadata
- Authors
- Erba, E., Bergamaschi, D., Bassano, L., Damia, G., Ronzoni, S., Faircloth, G. T., & D'Incalci, M.
- Affiliations
- Mario Negri Institute for Pharmacological Research (IT)
- Rayonix (United States) (US)
- Corresponding author
- Erba, E
- Venue
- European Journal of Cancer
- Publisher
- Elsevier BV
- Published
- 2001-01
- Volume
- 37
- Issue
- 1
- Pages
- 97-105
- ISSN
- 0959-8049 (ISSN-L)
- OpenAlex
- W2153737617
- Cited by
- 262
- References
- 28
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 7 · 2023: 7 · 2022: 8 · 2021: 7 · 2020: 6 · 2019: 6 · 2018: 6 · 2017: 8 · 2016: 10 · 2015: 21 · 2014: 19 · 2013: 9 · 2012: 4
- FWCI
- 6.19
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Cancer (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Cancer Research Institute
- Associazione Italiana per la Ricerca sul Cancro
- Topics
- Physical Sciences › Chemistry › Organic Chemistry › Isoquinoline Alkaloid Synthesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer therapeutics and mechanisms
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
- Keywords
- trabectedin, Ecteinascidia turbinata, cell cycle arrest, p53, nucleotide excision repair, ERCC1, DNA damage, DNA-protein crosslinks, ovarian cancer cell lines, drug resistance
- MeSH terms
- Trabectedin, Cell Cycle, Cell Division, Colonic Neoplasms, Dioxoles, DNA Damage, DNA, Neoplasm, Drug Screening Assays, Antitumor, Humans, Isoquinolines, Tumor Cells, Cultured, Tumor Suppressor Protein p53, Cyclins, Antineoplastic Agents, Alkylating, Tetrahydroisoquinolines
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