ArticleOncotarget2017
Novel post-transcriptional and post-translational regulation of pro-apoptotic protein BOK and anti-apoptotic protein Mcl-1 determine the fate of breast cancer cells to survive or die.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Low Expression of a Circular Transcript of the Apoptosis Regulator GeneBiomedicines · 2026Article
- Low BOK Expression Promotes Epithelial-Mesenchymal Transition and Migration via the Wnt Signaling Pathway in Breast Cancer Cells.International journal of molecular sciences · 2025Article
- MLKL regulates radiation-induced death in breast cancer cells: an interplay between apoptotic and necroptotic signals.Medical oncology (Northwood, London, England) · 2024Article
- Hispidulin: a promising anticancer agent and mechanistic breakthrough for targeted cancer therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Bok: real killer or bystander with non-apoptotic roles?Frontiers in cell and developmental biology · 2023Review
- Regulation of TRANK1 by GSK-3 in the brain: unexpected interactions.Molecular psychiatry · 2021Article
- Oxygen sensing, mitochondrial biology and experimental therapeutics for pulmonary hypertension and cancer.Free radical biology & medicine · 2021Article
- Mcl-1 and Bok transmembrane domains: Unexpected players in the modulation of apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The BCL-2 selective inhibitor ABT-199 sensitizes soft tissue sarcomas to proteasome inhibition by a concerted mechanism requiring BAX and NOXA.Cell death & disease · 2020Article
- The Multifaceted Roles of the BCL-2 Family Member BOK.Frontiers in cell and developmental biology · 2020Review
- Role of B-Cell Lymphoma 2 Ovarian Killer (BOK) in Acute Toxicity of Human Lung Epithelial Cells Caused by Cadmium Chloride.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Understanding Apoptosis and Apoptotic Pathways Targeted Cancer Therapeutics.Advanced pharmaceutical bulletin · 2019Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Deregulation of apoptosis is central to cancer progression and a major obstacle to effective treatment. The Bcl-2 gene family members play important roles in the regulation of apoptosis and are frequently altered in cancers. One such member is pro-apoptotic protein Bcl-2-related Ovarian Killer (BOK). Despite its critical role in apoptosis, the regulation of BOK expression is poorly understood in cancers. Here, we discovered that miR-296-5p regulates BOK expression by binding to its 3'-UTR in breast cancers. Interestingly, miR-296-5p also regulates the expression of anti-apoptotic protein myeloid cell leukemia 1 (Mcl-1), which is highly expressed in breast cancers. Our results reveal that Mcl-1 and BOK constitute a regulatory feedback loop as ectopic BOK expression induces Mcl-1, whereas silencing of Mcl-1 results in reduced BOK levels in breast cancer cells. In addition, we show that silencing of Mcl-1 but not BOK reduced the long-term growth of breast cancer cells. Silencing of both Mcl-1 and BOK rescued the effect of Mcl-1 silencing on breast cancer cell growth, suggesting that BOK is important for attenuating cell growth in the absence of Mcl-1. Depletion of BOK suppressed caspase-3 activation in the presence of paclitaxel and in turn protected cells from paclitaxel-induced apoptosis. Furthermore, we demonstrate that glycogen synthase kinase (GSK3) α/β interacts with BOK and regulates its level post-translationally in breast cancer cells. Taken together, our results suggest that fine tuning of the levels of pro-apoptotic protein BOK and anti-apoptotic protein Mcl-1 may decide the fate of cancer cells to either undergo apoptosis or proliferation.
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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.