ArticleJournal of cellular biochemistry2016
Anacardic Acid, Salicylic Acid, and Oleic Acid Differentially Alter Cellular Bioenergetic Function in Breast Cancer Cells.
Article in Journal of cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Long-Chain Fatty Acids Alter Estrogen Receptor Expression in Breast Cancer Cells.International journal of molecular sciences · 2025Article
- Viability of HepG2 and MCF-7 cells is not correlated with mitochondrial bioenergetics.Scientific reports · 2023Article
- Article
- Anacardium Occidentale L. Leaf Extracts Protect Against Glutamate/HFrontiers in pharmacology · 2021Article
- Anacardic acid mitigates liver fat accumulation and impaired glucose tolerance in mice fed a high-fat and high-sucrose diet.Food science & nutrition · 2020Article
- Mitochondria-targeted triphenylphosphonium-based compounds do not affect estrogen receptor α.PeerJ · 2020Article
- Article
- Transcriptomic response of breast cancer cells to anacardic acid.Scientific reports · 2018Article
- Article
- Synthesis and in vitro biological evaluation of thiosulfinate derivatives for the treatment of human multidrug-resistant breast cancer.Acta pharmacologica Sinica · 2017Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Anacardic acid is a dietary and medicinal phytochemical that inhibits breast cancer cell proliferation and uncouples oxidative phosphorylation (OXPHOS) in isolated rat liver mitochondria. Since mitochondrial-targeted anticancer therapy (mitocans) may be useful in breast cancer, we examined the effect of anacardic acid on cellular bioenergetics and OXPHOS pathway proteins in breast cancer cells modeling progression to endocrine-independence: MCF-7 estrogen receptor α (ERα)+ endocrine-sensitive; LCC9 and LY2 ERα+, endocrine-resistant, and MDA-MB-231 triple negative breast cancer (TNBC) cells. At concentrations similar to cell proliferation IC50 s, anacardic acid reduced ATP-linked oxygen consumption rate (OCR), mitochondrial reserve capacity, and coupling efficiency while increasing proton leak, reflecting mitochondrial toxicity which was greater in MCF-7 compared to endocrine-resistant and TNBC cells. These results suggest tolerance in endocrine-resistant and TNBC cells to mitochondrial stress induced by anacardic acid. Since anacardic acid is an alkylated 2-hydroxybenzoic acid, the effects of salicylic acid (SA, 2-hydroxybenzoic acid moiety) and oleic acid (OA, monounsaturated alkyl moiety) were tested. SA inhibited whereas OA stimulated cell viability. In contrast to stimulation of basal OCR by anacardic acid (uncoupling effect), neither SA nor OA altered basal OCR- except OA inhibited basal and ATP-linked OCR, and increased ECAR, in MDA-MB-231 cells. Changes in OXPHOS proteins correlated with changes in OCR. Overall, neither the 2-hydroxybenzoic acid moiety nor the monounsaturated alky moiety of anacardic acid is solely responsible for the observed mitochondria-targeted anticancer activity in breast cancer cells and hence both moieties are required in the same molecule for the observed effects. J. Cell. Biochem. 117: 2521-2532, 2016. © 2016 Wiley Periodicals, Inc.
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Registered trials
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