ArticleOncotarget2017
Mcl-1 regulates reactive oxygen species via NOX4 during chemotherapy-induced senescence.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
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- Targeting the redox-programmed cell death axis in breast cancer: from molecular mechanisms to therapeutic resistance.Cell death discovery · 2025Review
- Targeting MCL-1 to Overcome Therapeutic Resistance and Improve Cancer Mortality.Health science reports · 2025Article
- MCL1 may not mediate chemoresistance.bioRxiv : the preprint server for biology · 2025Article
- Antioxidant Senotherapy by Natural Compounds: A Beneficial Partner in Cancer Treatment.Antioxidants (Basel, Switzerland) · 2025Review
- Oxidative cell death in cancer: mechanisms and therapeutic opportunities.Cell death & disease · 2024Review
- Hippo Signaling Pathway in Colorectal Cancer: Modulation by Various Signals and Therapeutic Potential.Analytical cellular pathology (Amsterdam) · 2024Review
- Involvement of Bcl-2 Family Proteins in Tetraploidization-Related Senescence.International journal of molecular sciences · 2023Review
- Understanding MCL1: from cellular function and regulation to pharmacological inhibition.The FEBS journal · 2022Review
- Metabolic Adaptation-Mediated Cancer Survival and Progression in Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Oridonin enhances antitumor effects of doxorubicin in human osteosarcoma cells.Pharmacological reports : PR · 2022Article
- MCL1 nuclear translocation induces chemoresistance in colorectal carcinoma.Cell death & disease · 2022Article
- miR-340-5p Mediates Cardiomyocyte Oxidative Stress in Diabetes-Induced Cardiac Dysfunction by Targeting Mcl-1.Oxidative medicine and cellular longevity · 2022Article
- Breast cancer dependence on MCL-1 is due to its canonical anti-apoptotic function.Cell death and differentiation · 2021Article
- The Role of Oxidative Stress and Its Counteractive Utility in Colorectal Cancer (CRC).Cancers · 2020Review
- Phosphoinositide 3-Kinase/Akt Signaling and Redox Metabolism in Cancer.Frontiers in oncology · 2018Review
- microRNA-802 is involved in palmitate-induced damage to pancreatic β cells through repression of sirtuin 6.International journal of clinical and experimental pathology · 2017Article
- Targeting MUC1-C suppresses BCL2A1 in triple-negative breast cancer.Signal transduction and targeted therapyArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mcl-1, a Bcl-2 family member, is highly expressed in a variety of human cancers and is believed to enhance tumorigenic potential and chemotherapy resistance through the inhibition of apoptosis and senescence. We previously reported that Mcl-1's regulation of chemotherapy-induced senescence (CIS) is dependent on its ability to prevent reactive oxygen species (ROS) generation. In this report, we demonstrate that Mcl-1-regulated CIS requires not only ROS, but specifically mitochondrial ROS, and that these events are upstream of activation of the DNA damage response, another necessary step toward senescence. Mcl-1's anti-senescence activity also involves the unique ability to inhibit ROS formation by preventing the upregulation of pro-oxidants. Specifically, we found that NADPH oxidases (NOXs) are regulated by Mcl-1 and that NOX4 expression in particular is a required step for CIS induction that is blocked by Mcl-1. Lastly, we illustrate that by preventing expression of NOX4, Mcl-1 limits its availability in the mitochondria, thereby lowering the production of mitochondrial ROS during CIS. Our studies not only define the essential role of Mcl-1 in chemoresistance, but also for the first time link a key pro-survival Bcl-2 family member with the NOX protein family, both of which have significant ramifications in cancer progression.
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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 OpenQuestion graph.