ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2013
Induction of apoptosis by Trichostatin A in human breast cancer cell lines: involvement of 15-Lox-1.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Transfection of 12/15-lipoxygenase effectively alleviates inflammatory responses during experimental acute pancreatitis.World journal of gastroenterology · 2024Article
- Lipoxygenases at the Intersection of Infection and Carcinogenesis.International journal of molecular sciences · 2024Review
- Review
- Pharmacological Properties of Trichostatin A, Focusing on the Anticancer Potential: A Comprehensive Review.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Hormonal and Genetic Regulatory Events in Breast Cancer and Its Therapeutics: Importance of the Steroidogenic Acute Regulatory Protein.Biomedicines · 2022Review
- Evaluation of the expression of necroptosis pathway mediators and its association with tumor characteristics in functional and non-functional pituitary adenomas.BMC endocrine disorders · 2022Article
- 15-Lipoxygenase and its metabolites in the pathogenesis of breast cancer: A double-edged sword.Lipids in health and disease · 2021Review
- Structurally Diverse Histone Deacetylase Photoreactive Probes: Design, Synthesis, and Photolabeling Studies in Live Cells and Tissue.ChemMedChem · 2019Article
- Implications of dietary ω-3 and ω-6 polyunsaturated fatty acids in breast cancer.Experimental and therapeutic medicine · 2018Article
- Sodium butyrate promotes apoptosis in breast cancer cells through reactive oxygen species (ROS) formation and mitochondrial impairment.Lipids in health and disease · 2017Article
- Article
- Involvement of 15-lipoxygenase-1 in the regulation of breast cancer cell death induced by sodium butyrate.Cytotechnology · 2016Article
- Evaluation of RIP1K and RIP3K expressions in the malignant and benign breast tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- A gene-signature progression approach to identifying candidate small-molecule cancer therapeutics with connectivity mapping.BMC bioinformatics · 2016Article
- RIP1K and RIP3K provoked by shikonin induce cell cycle arrest in the triple negative breast cancer cell line, MDA-MB-468: necroptosis as a desperate programmed suicide pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Mammalian lipoxygenases and their biological relevance.Biochimica et biophysica acta · 2015Review
- BRCA-Monet: a breast cancer specific drug treatment mode-of-action network for treatment effective prediction using large scale microarray database.BMC systems biology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
15-Lipoxygenase-1 (15-Lox-1) is a key enzyme mediating oxidative metabolism of polyunsaturated fatty acids and has attracted considerable interest as a potential target for the induction of apoptosis in cancer cells. Knowledge of relationship between 15-Lox-1 and histone deacetylase inhibitors is lacking in the breast cancer. This study is aimed to investigate the role of Trichostatin A (TSA) and 13(S)-HODE, as a metabolite of 15-Lox-1, in the regulation of breast cancer cell growth. The cytotoxic effect of TSA, as a potent HDAC inhibitor, was measured using MTT assay. Annexin V-FITC and PI staining were performed to detect apoptosis and cell cycle distribution using Flow cytometry. The role of 15-Lox-1 in the regulation of cell growth was assessed by 15-Lox-1 inhibitor and the level of 15-Lox-1 metabolite was measured to determine 15-Lox activity after treatment by TSA. The results demonstrated that TSA induced cell growth inhibition via 15-Lox-1, in a dose- and time-dependent manner, and subsequently accompanied by the cell cycle arrest and induction of apoptosis. Moreover, growth inhibitory effect of TSA was associated with the elevation of 15-Lox-1 metabolite (13(S)-HODE). This study provided evidences that the inhibitory effect of TSA on the breast cancer cell growth occurs via the induction of 15-Lox-1 activity and 13(S)-HODE production. Our findings underline the possible role of 15-Lox-1/13(S)-HODE pathway as a promising molecular approach for the induction of apoptosis in breast cancer cells.
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