ArticlePloS one2013
Proteasomal degradation of Mcl-1 by maritoclax induces apoptosis and enhances the efficacy of ABT-737 in melanoma cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Broad-Spectrum Anti-Infective Activity of Natural Compounds Pyrrolomycins, Marinopyrroles, and Their Analogs.Pathogens (Basel, Switzerland) · 2026Review
- Saga of MCL1 inhibitors in multiple myeloma.Biochemical pharmacology · 2026Review
- Maritoclax Overcomes FBW7 Deficiency-Driven Irinotecan Resistance in Colorectal Cancer by Targeting MCL1.Cancer medicine · 2025Article
- Cancer Cell Cytotoxicity of Marinopyrroles, Pyrrolomycins, and Their Derivatives.Marine drugs · 2025Review
- Expanded Gram-Negative Activity of Marinopyrrole A.Pathogens (Basel, Switzerland) · 2025Article
- Resolving the current controversy of use and reuse of housekeeping proteins in ageing research: Focus on saving people's tax dollars.Ageing research reviews · 2024Review
- KS18, a Mcl-1 inhibitor, improves the effectiveness of bortezomib and overcomes resistance in refractory multiple myeloma by triggering intrinsic apoptosis.Frontiers in pharmacology · 2024Article
- Past, Present, and a Glance into the Future of Multiple Myeloma Treatment.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Small-molecule High-throughput Screening Identifies an MEK Inhibitor PD198306 that Enhances Sorafenib Efficacy via MCL-1 and BIM in Hepatocellular Carcinoma Cells.Combinatorial chemistry & high throughput screening · 2023Article
- Non-coding RNA-related antitumor mechanisms of marine-derived agents.Frontiers in pharmacology · 2022Review
- Mcl-1 Inhibition: Managing Malignancy in Multiple Myeloma.Frontiers in pharmacology · 2021Review
- Single Agent and Synergistic Activity of Maritoclax with ABT-263 in Nasopharyngeal Carcinoma (NPC) Cell Lines.Tropical life sciences research · 2020Article
- AMG-176, an Mcl-1 Antagonist, Shows Preclinical Efficacy in Chronic Lymphocytic Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Article
- Maritoclax Enhances TRAIL-Induced Apoptosis via CHOP-Mediated Upregulation of DR5 and miR-708-Mediated Downregulation of cFLIP.Molecules (Basel, Switzerland) · 2018Article
- YM155 enhances ABT-737-mediated apoptosis through Mcl-1 downregulation in Mcl-1-overexpressed cancer cells.Molecular and cellular biochemistry · 2017Article
- Virtual screening for potential inhibitors of Mcl-1 conformations sampled by normal modes, molecular dynamics, and nuclear magnetic resonance.Drug design, development and therapy · 2017Article
- Targeting Cell Survival Proteins for Cancer Cell Death.Pharmaceuticals (Basel, Switzerland) · 2016Review
- Leukemia inhibitory factor protects cholangiocarcinoma cells from drug-induced apoptosis via a PI3K/AKT-dependent Mcl-1 activation.Oncotarget · 2015Article
- Maritoclax and dinaciclib inhibit MCL-1 activity and induce apoptosis in both a MCL-1-dependent and -independent manner.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeMetastatic melanoma remains one of the most invasive and highly drug resistant cancers. The over expression of anti-apoptotic protein Mcl-1 has been associated with inferior survival, poor prognosis and chemoresistance of malignant melanoma. A BH3 mimetic, ABT-737, has demonstrated efficacy in several forms of cancers. However, the efficacy of ABT-737 depends on Mcl-1. Because the over expression of Mcl-1 is frequently observed in melanoma, specifically targeting of Mcl-1 may overcome the resistance of ABT-737. In this study, we investigated the effects of Maritoclax, a novel Mcl-1-selective inhibitor, alone and in combination with ABT-737, on the survival of human melanoma cells. EXPERIMENTAL APPROACH: For cell viability assessment we performed MTT assay. Apoptosis was determined using western blot and flow cytometric analysis. KEY
resultsThe treatment of Maritoclax reduced the cell viability of melanoma cells with an IC50 of between 2.2-5.0 µM. Further, treatment of melanoma cells with Maritoclax showed significant decrease in Mcl-1 expression. We found that Maritoclax was able to induce apoptosis in melanoma cells in a caspase-dependent manner. Moreover, Maritoclax induced Mcl-1 degradation via the proteasome system, which was associated with its pro-apoptotic activity. We also found that Maritoclax treatment increased mitochondrial translocation of Bim and Bmf. Importantly, Maritoclax markedly enhanced the efficacy of ABT-737 against melanoma cells in both two- and three-dimensional spheroids. CONCLUSIONS AND IMPLICATIONS: Taken together, these results suggest that targeting of Mcl-1 by Maritoclax may represent a new therapeutic strategy for melanoma treatment that warrants further investigation as a single therapy or in combination with other agents such as Bcl-2 inhibitors.
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