ArticleCell death & disease2020
BIK drives an aggressive breast cancer phenotype through sublethal apoptosis and predicts poor prognosis of ER-positive breast cancer.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Anastasis: an unwelcome guest in cancer therapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Apoptosis gene expression analysis identifies biologically distinct AML clusters and BIK as an independent prognostic marker.Annals of hematology · 2026Article
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Apoptotic Signaling Across Breast Cancer Subtypes and Cryoablation-Induced Tissue Injury.International journal of molecular sciences · 2026Article
- Targeting microRNA let-7b-5p-mediated aberrant androgen receptor signaling for prevention of hormone receptor-negative breast cancer.NPJ breast cancer · 2026Article
- Reactive oxygen species (ROS) in cancer: from mechanism to therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Genes Associated with Apoptosis in an Experimental Breast Cancer Model.International journal of molecular sciences · 2025Article
- A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025Review
- Prognosis of cholangiocarcinoma patients based on multiple patterns of programmed cell death, integrated analysis of the immune microenvironment and drug sensitivity.Frontiers in genetics · 2025Article
- Comparing the BAD Protein Interactomes in 2D and 3D Cell Culture Using Proximity Labeling.Journal of proteome research · 2024Article
- MyoD1 promotes the transcription of BIK and plays an apoptosis-promoting role in the development of gastric cancer.Cell cycle (Georgetown, Tex.) · 2024Article
- Targeted Single-cell Isolation of Spontaneously Escaping Live Melanoma Cells for Comparative Transcriptomics.Cancer research communications · 2023Article
- De Novo Design of Imidazopyridine-Tethered Pyrazolines That Target Phosphorylation of STAT3 in Human Breast Cancer Cells.Bioengineering (Basel, Switzerland) · 2023Article
- Deciphering the Hypoxia-immune interface in esophageal squamous carcinoma: a prognostic network model.Frontiers in oncology · 2023Article
- Spontaneous activity of the mitochondrial apoptosis pathway drives chromosomal defects, the appearance of micronuclei and cancer metastasis through the Caspase-Activated DNAse.Cell death & disease · 2022Article
- Regulation of Bcl-2 Family Proteins in Estrogen Receptor-Positive Breast Cancer and Their Implications in Endocrine Therapy.Cancers · 2022Review
- Identification of BIK as an unfavorable prognostic marker and novel therapeutic target in microsatellite stable colorectal cancer harboring KRAS mutations.American journal of cancer research · 2022Article
- Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts.International journal of molecular sciences · 2021Review
- Apoptosis - Fueling the oncogenic fire.The FEBS journal · 2021Review
- Mutagenic Consequences of Sublethal Cell Death Signaling.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis is fundamental to normal animal development and is the target for many anticancer therapies. Recent studies have explored the consequences of "failed apoptosis" where the apoptotic program is initiated but does not go to completion and does not cause cell death. Nevertheless, this failed apoptosis induces DNA double-strand breaks generating mutations that facilitate tumorigenesis. Whether failed apoptosis is relevant to clinical disease is unknown. BCL-2 interacting killer (BIK) is a stress-induced BH3-only protein that stimulates apoptosis in response to hormone and growth factor deprivation, hypoxia, and genomic stress. It was unclear whether BIK promotes or suppresses tumor survival within the context of breast cancer. We investigated this and show that BIK induces failed apoptosis with limited caspase activation and genomic damage in the absence of extensive cell death. Surviving cells acquire aggressive phenotypes characterized by enrichment of cancer stem-like cells, increased motility and increased clonogenic survival. Furthermore, by examining six independent cohorts of patients (total n = 969), we discovered that high BIK mRNA and protein levels predicted clinical relapse of Estrogen receptor (ER)-positive cancers, which account for almost 70% of all breast cancers diagnosed but had no predictive value for hormone receptor-negative (triple-negative) patients. Thus, this study identifies BIK as a biomarker for tumor recurrence of ER-positive patients and provides a potential mechanism whereby failed apoptosis contributes to cancer aggression.
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