ArticleBMC cancer2025
Excavatolide C has oxidative-stress-dependent antiproliferative and apoptotic effects against breast cancer cells.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
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Who cites it
4 citing papers in PubMed.
- A Pyrone Glucoside fromBiomolecules · 2026Article
- Cryptocaryone Exhibits ROS/MAPK-Dependent Antiproliferative and Apoptosis-Inducing Effects on Triple-Negative Breast Cancer Cells and Proof-of-Concept Breast Cancer Mouse Model.Drug development research · 2026Article
- Excavatolide E triggers oxidative stress-associated apoptosis and DNA damage to inhibit bladder cancer cell proliferation.Molecular biology reports · 2025Article
- Nanoarchaeosomes for synergistic photochemotherapy in triple-negative breast cancer.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundTriple negative breast cancer (TNBC) shows a poor response to targeted therapy drugs for non-triple-negative breast cancer (non-TNBC). Developing anticancer drugs that are effective for both TNBC and non-TNBC cells is necessary. The marine coral Briareum excavatum-derived excavatolide C (EXCC) exhibits anti-bladder cancer cell proliferation. However, the anti-breast cancer properties and drug safety of are unclear.
methodsThis study aimed to evaluate the antiproliferative effect and mechanisms (oxidative stress, DNA damage, and apoptosis) caused by EXCC on TNBC and non-TNBC cells in parallel with normal cells.
resultsEXCC demonstrated higher antiproliferative effects in various breast cancer cell lines (MDA-MB-231, Hs578t, MDA-MB-468, and MCF7) than in normal breast cell lines (H184B5F5/M10; M10) as detected in a 48 h ATP assay. MDA-MB-231 and MCF7 were chosen as representative TNBC and non-TNBC cells, respectively, to clarify the underlying molecular mechanisms. EXCC highly upregulated reactive oxygen species and mitochondrial superoxide, reduced the mitochondrial membrane potential, and downregulated glutathione in breast cancer compared with normal cells. These EXCC-triggered antiproliferative and oxidative stress changes were attenuated by the ROS inhibitor N-acetylcysteine (NAC). Consistently, in breast cancer cells, EXCC triggered subG1 accumulation, apoptosis, caspase activation, and DNA damage (γH2AX and 8-hydroxy-2'-deoxyguanosine), all of which were alleviated by NAC.
conclusionOverall, the antiproliferative effects and molecular mechanisms caused by EXCC in breast cancer treatment depend on oxidative stress. Without cytotoxicity to normal cells, EXCC is a potential antiproliferative marine natural product for TNBC and non-TNBC cells.
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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 Socratic graph.