ArticleMolecular carcinogenesis2009
Targeted disruption of Bcl-xL in mouse keratinocytes inhibits both UVB- and chemically induced skin carcinogenesis.
Article in Molecular carcinogenesis, 2009. 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, 36 citations in OpenAlex.
- MCL‑1 safeguards activated hair follicle stem cells to enable adult hair regeneration.Nature communications · 2025Article
- Ultraviolet Radiation Exposure and its Impacts on Cutaneous Phosphorylation Signaling in Carcinogenesis: Focusing on Protein Tyrosine PhosphatasesPhotochemistry and photobiology · 2023Review
- The Aryl Hydrocarbon Receptor in the Pathogenesis of Environmentally-Induced Squamous Cell Carcinomas of the Skin.Frontiers in oncology · 2022Review
- Overexpression of Stat3 increases circulating cfDNA in breast cancer.Breast cancer research and treatment · 2021Article
- Molecular signaling cascades involved in nonmelanoma skin carcinogenesis.The Biochemical journal · 2016Review
- Negative regulation of the FOXO3a transcription factor by mTORC2 induces a pro-survival response following exposure to ultraviolet-B irradiation.Cellular signalling · 2016Article
- Chronic Inflammation in Skin Malignancies.Journal of molecular signaling · 2016Review
- Twist1 regulates keratinocyte proliferation and skin tumor promotion.Molecular carcinogenesis · 2016Article
- Endogenous Sterol Metabolites Regulate Growth of EGFR/KRAS-Dependent Tumors via LXR.Cell reports · 2015Article
- Lessons from gain- and loss-of-function models of pro-survival Bcl2 family proteins: implications for targeted therapy.The FEBS journal · 2015Review
- Metformin inhibits skin tumor promotion in overweight and obese mice.Cancer prevention research (Philadelphia, Pa.) · 2014Article
- Role of stat3 in skin carcinogenesis: insights gained from relevant mouse models.Journal of skin cancer · 2013Article
- Inhibition of mTOR suppresses UVB-induced keratinocyte proliferation and survival.Cancer prevention research (Philadelphia, Pa.) · 2012Article
- Development and homeostasis of the skin epidermis.Cold Spring Harbor perspectives in biology · 2012Article
- Glutathione peroxidase-1 in health and disease: from molecular mechanisms to therapeutic opportunities.Antioxidants & redox signaling · 2011Review
- Establishment of a transgenic zebrafish line for superficial skin ablation and functional validation of apoptosis modulators in vivo.PloS one · 2011Article
- Bcl-2 and accelerated DNA repair mediates resistance of hair follicle bulge stem cells to DNA-damage-induced cell death.Nature cell biology · 2010Article
- The insulin-like growth factor (IGF)-I E-peptides are required for isoform-specific gene expression and muscle hypertrophy after local IGF-I production.Journal of applied physiology (Bethesda, Md. : 1985) · 2010Article
- Targeted disruption of stat3 reveals a major role for follicular stem cells in skin tumor initiation.Cancer research · 2009Article
- Multi-stage chemical carcinogenesis in mouse skin: fundamentals and applications.Nature protocols · 2009Article
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 2 institutions in 2 countries.
Funding
Abstract
Bcl-x(L) is one of several antiapoptotic proteins regulated by signal transducer and activator of transcription 3 (Stat3). We have recently shown that Stat3 is required for chemically induced and ultraviolet B (UVB)-induced skin carcinogenesis. In this study, the functional role of Bcl-x(L) in skin carcinogenesis was investigated using skin-specific Bcl-x(L)-deficient mice. In this model, Bcl-x(L) expression is disrupted in the basal compartment of mouse epidermis using the bovine keratin 5 (K5) promoter to drive expression of Cre recombinase (K5.Cre x Bcl-x(L) (fl/fl) mice). A significant increase in apoptosis induced by either UVB irradiation or 7,12-dimethylbenz[a]anthracene (DMBA) treatment was observed in the epidermis of Bcl-x(L)-deficient mice. Furthermore, an increase in apoptotic cells was noted in hair follicle keratinocytes, including those located in the bulge region. Cell proliferation was not affected by Bcl-x(L) deficiency following exposure to either UVB or 12-O-tetradecanoylphorbol-13-acetate (TPA). Bcl-x(L)-deficient mice were more resistant than wild-type controls to skin tumor development with delayed onset and reduced number of tumors using either UVB or the DMBA/TPA two-stage regimen. Moreover, Bcl-2, Mcl-1, and survivin protein levels were increased in the epidermis of Bcl-x(L)-deficient mice in the absence of stimuli. Furthermore, levels of these antiapoptotic proteins were also high in skin tumors from Bcl-x(L)-deficient mice that developed in response to either UVB or two-stage carcinogenesis protocols. Collectively, these studies demonstrate that Bcl-x(L) plays a role early in skin carcinogenesis through its anti-apoptotic functions to enhance survival of keratinocytes, including bulge region keratinocyte stem cells, following DNA damage.
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What OpenQuestion holds
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.