ArticleCell death & disease2012
MS-275 sensitizes osteosarcoma cells to Fas ligand-induced cell death by increasing the localization of Fas in membrane lipid rafts.
Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Employing splice-switching oligonucleotides and AAVrh74.U7 snRNA to target insulin receptor splicing and cancer hallmarks in osteosarcoma.Molecular therapy. Oncology · 2024Article
- Cholesterol-enriched membrane micro-domaindeficiency induces doxorubicin resistancevia promoting autophagy in breast cancer.Molecular therapy oncolytics · 2021Article
- Prospects for NK Cell Therapy of Sarcoma.Cancers · 2020Review
- Lipid rafts as signaling hubs in cancer cell survival/death and invasion: implications in tumor progression and therapy: Thematic Review Series: Biology of Lipid Rafts.Journal of lipid research · 2020Review
- Natural Killer Cell Immunotherapy for Osteosarcoma.Advances in experimental medicine and biology · 2020Review
- Innate Immune Cells: A Potential and Promising Cell Population for Treating Osteosarcoma.Frontiers in immunology · 2019Review
- Expression patterns of class I histone deacetylases in osteosarcoma: a novel prognostic marker with potential therapeutic implications.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018Article
- miR-20a Regulates FAS Expression in Osteosarcoma Cells by ModulatingMolecular cancer therapeutics · 2018Article
- Droxinostat sensitizes human colon cancer cells to apoptotic cell death via induction of oxidative stress.Cellular & molecular biology letters · 2018Article
- Therapeutic applications of histone deacetylase inhibitors in sarcoma.Cancer treatment reviews · 2017Review
- Energy sensing pathways: Bridging type 2 diabetes and colorectal cancer?Journal of diabetes and its complications · 2017Review
- Bone microenvironment signals in osteosarcoma development.Cellular and molecular life sciences : CMLS · 2015Review
- Anticancer activity of MPT0G157, a derivative of indolylbenzenesulfonamide, inhibits tumor growth and angiogenesis.Oncotarget · 2015Article
- The narrow-spectrum HDAC inhibitor entinostat enhances NKG2D expression without NK cell toxicity, leading to enhanced recognition of cancer cells.Pharmaceutical research · 2015Article
- Osteosarcoma Genetics and Epigenetics: Emerging Biology and Candidate Therapies.Critical reviews in oncogenesis · 2015Review
- Expression of c-FLIP in pulmonary metastases in osteosarcoma patients and human xenografts.Pediatric blood & cancer · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Fas expression is inversely correlated with the metastatic potential of osteosarcoma (OS) cells to the lungs. Fas⁺ cells are rapidly eliminated when they enter the lungs via their interaction with constitutive Fas ligand (FasL) on the lung epithelium, whereas Fas⁻ OS cells escape this FasL-induced apoptosis and survive in the lung microenvironment. Upregulation of Fas expression in established OS lung metastases results in tumor regression. Here, we demonstrate that treatment of Fas⁻ OS cells with the histone deacetylase inhibitor MS-275 results in the upregulation of Fas mRNA and sensitizes these cells to FasL-induced apoptosis. However, flow cytometry analysis revealed that Fas cell surface protein expression was not significantly increased. Rather, we observed increased levels of Fas within the membrane lipid rafts, as demonstrated by an increase in Fas expression in detergent-insoluble lipid raft fractions and colocalization with GM1⁺ lipid rafts. We had previously shown that MS-275 treatment inhibited expression of the anti-apoptotic cellular FLICE-inhibitory protein (c-FLIP). Here, we demonstrated that transfection of cells with short hairpin RNA to c-FLIP also resulted in the localization of Fas to lipid rafts. Overall, our studies indicate that MS-275 sensitizes OS cells to FasL by upregulating the expression of Fas in membrane lipid rafts, which correlates with the c-FLIP-dependent distribution of Fas to lipid rafts.
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