ArticleOncogene1999
Targeted expression of c-Myc in the epidermis alters normal proliferation, differentiation and UV-B induced apoptosis.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 73 citations in OpenAlex.
- HDAC1/2 Control Proliferation and Survival in Adult Epidermis and Pre‒Basal Cell Carcinoma through p16 and p53.The Journal of investigative dermatology · 2022Article
- NGS Analysis Confirms CommonInternational journal of molecular sciences · 2021Article
- c-Myc Upregulated by High Glucose Inhibits HaCaT Differentiation by S100A6 Transcriptional Activation.Frontiers in endocrinology · 2021Article
- Article
- Unraveling cancer lineage drivers in squamous cell carcinomas.Pharmacology & therapeutics · 2020Review
- Review
- Enhancement of Cutaneous Wound Healing by Dsg2 Augmentation of uPAR Secretion.The Journal of investigative dermatology · 2018Article
- FOXM1 allows human keratinocytes to bypass the oncogene-induced differentiation checkpoint in response to gain of MYC or loss of p53.Oncogene · 2017Article
- Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.Biochimica et biophysica acta · 2015Review
- Palatogenesis and cutaneous repair: A two-headed coin.Developmental dynamics : an official publication of the American Association of Anatomists · 2015Review
- Mechanisms regulating epidermal stem cells.The EMBO journal · 2012Review
- Skp2 is necessary for Myc-induced keratinocyte proliferation but dispensable for Myc oncogenic activity in the oral epithelium.The American journal of pathology · 2011Article
- Ovol2 suppresses cell cycling and terminal differentiation of keratinocytes by directly repressing c-Myc and Notch1.The Journal of biological chemistry · 2009Article
- Opposing effects of KLF5 on the transcription of MYC in epithelial proliferation in the context of transforming growth factor beta.The Journal of biological chemistry · 2009Article
- Dual role of COUP-TF-interacting protein 2 in epidermal homeostasis and permeability barrier formation.The Journal of investigative dermatology · 2009Article
- Disruption of epidermal specific gene expression and delayed skin development in AP-2 gamma mutant mice.Developmental biology · 2008Article
- MYC in mammalian epidermis: how can an oncogene stimulate differentiation?Nature reviews. Cancer · 2008Review
- Pemphigus vulgaris identifies plakoglobin as key suppressor of c-Myc in the skin.The EMBO journal · 2006Article
- Deregulated minichromosomal maintenance protein MCM7 contributes to oncogene driven tumorigenesis.Oncogene · 2006Article
- Ovol1 regulates the growth arrest of embryonic epidermal progenitor cells and represses c-myc transcription.The Journal of cell biology · 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
3 authors at 1 institution in 1 country.
Funding
Abstract
c-Myc overexpression has been associated with several types of human cancers. To study the role of c-myc in epidermal differentiation and carcinogenesis, a transgenic mouse model was created to overexpress c-Myc in the epidermis. Human c-myc 2 cDNA was subcloned into a 6.5 kb mouse loricrin expression vector, ML.myc2. This loricrin promoter primarily directs expression in the epidermis in both proliferating and differentiated keratinocytes. On day 4, ML.myc2 transgenic pups develop a hyperkeratotic phenotype, which progressively worsens until day 7. Upon histological analysis, both hyperplasia and hyperkeratosis were evident. Bromodeoxyuridine (BrdU) incorporation revealed that transgenic mice had a threefold increase in the number of proliferating cells as compared with a normal littermate. Proliferative cells in the ML.myc2 epidermis were also found to be suprabasal, suggesting an inhibition of terminal differentiation in keratinocytes. Inhibition of terminal differentiation by c-Myc overexpression was further suggested by aberrant expression of differentiation markers, keratin 1, keratin 6, loricrin, and filaggrin in ML.myc2 transgenic mice. Interestingly, ML.myc2 keratinocytes exhibit a reduced sensitivity to UV-B induced apoptosis, in vivo. In vitro studies reveal the reduced sensitivity of ML.myc2 keratinocytes to UV-B irradiation is growth factor dependent. These findings provide evidence that overexpression of c-Myc in the epidermis induces proliferation, inhibits terminal differentiation and decreases the sensitivity of keratinocytes to UV-B induced apoptosis.
Indexed as
Identifiers
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.