ArticleOncogene2005
Caspase-independent induction of apoptosis in human melanoma cells by the proapoptotic Bcl-2-related protein Nbk / Bik.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 46 citations in OpenAlex.
- A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025Review
- BIK drives an aggressive breast cancer phenotype through sublethal apoptosis and predicts poor prognosis of ER-positive breast cancer.Cell death & disease · 2020Article
- Bik reduces hyperplastic cells by increasing Bak and activating DAPk1 to juxtapose ER and mitochondria.Nature communications · 2017Article
- Biphasic ROS production, p53 and BIK dictate the mode of cell death in response to DNA damage in colon cancer cells.PloS one · 2017Article
- Copy number variation in archival melanoma biopsies versus benign melanocytic lesions.Cancer biomarkers : section A of Disease markers · 2016Article
- Photosensitizing and radiosensitizing effects of mitoxantrone: combined chemo-, photo-, and radiotherapy of DFW human melanoma cells.Lasers in medical science · 2013Article
- The critical roles of endoplasmic reticulum chaperones and unfolded protein response in tumorigenesis and anticancer therapies.Oncogene · 2013Review
- Disruption of the VDAC2-Bak interaction by Bcl-x(S) mediates efficient induction of apoptosis in melanoma cells.Cell death and differentiation · 2012Article
- Mutual regulation of Bcl-2 proteins independent of the BH3 domain as shown by the BH3-lacking protein Bcl-x(AK).PloS one · 2012Article
- Novel mechanism of anti-apoptotic function of 78-kDa glucose-regulated protein (GRP78): endocrine resistance factor in breast cancer, through release of B-cell lymphoma 2 (BCL-2) from BCL-2-interacting killer (BIK).The Journal of biological chemistry · 2011Article
- BH3-only protein Bik is involved in both apoptosis induction and sensitivity to oxidative stress in multiple myeloma.British journal of cancer · 2010Article
- An ARF/CtBP2 complex regulates BH3-only gene expression and p53-independent apoptosis.Cell death and differentiation · 2010Article
- BIK, the founding member of the BH3-only family proteins: mechanisms of cell death and role in cancer and pathogenic processes.Oncogene · 2008Review
- Expression and function of bcl-2 proteins in melanoma.Current genomics · 2008Article
- Article
- BH3-only protein BIK induces caspase-independent cell death with autophagic features in Bcl-2 null cells.Oncogene · 2008Article
- Mcl-1 determines the Bax dependency of Nbk/Bik-induced apoptosis.The Journal of cell biology · 2007Article
- A novel Bcl-x splice product, Bcl-xAK, triggers apoptosis in human melanoma cells without BH3 domain.Oncogene · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proapoptotic BH3-only protein natural born killer / Bcl-2 interacting killer (Nbk/Bik) has been described to inhibit Bcl-2 and Bcl-xL, thereby supporting the death promoting ability of Bax. In order to evaluate its function in melanoma, we investigated the response after Nbk/Bik overexpression in cultured human melanoma cells and in a melanoma mouse model. Untransfected melanoma cell lines expressed Nbk/Bik only weakly at the mRNA and protein level. Conditional expression of Nbk/Bik by applying the inducible tetracycline-responsive expression system triggered apoptosis and enhanced sensitivity to proapoptotic stimuli as to agonistic CD95 activation and to chemotherapeutics etoposide, doxorubicin and pamidronate. For investigating the effects of Nbk/Bik in vivo, stably transfected melanoma cells were subcutaneously injected into nude mice. Significantly delayed tumor growth was the result when mice received doxycycline for induction of Nbk/Bik expression. By investigating the mechanism of Nbk/Bik-induced cell death, typical hallmarks of apoptosis such as DNA fragmentation and chromatin condensation were seen after induction. Interestingly, no indications for cytochrome c release and caspase processing were found, and selective caspase inhibition remained without effect. These data indicate the high potential of Nbk/Bik in regulating apoptosis in melanoma by a caspase-independent pathway and may corroborate the potency of novel antimelanoma strategies based on activation of BH3-only proteins such as Nbk/Bik.
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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.