A new stable line of human keratinocytes was obtained. The cells have altered morphology, both abnormal chromosomal composition and expression of keratinocyte markers, do not show contact inhibition, could be cultured in various media and have limited stratification ability in vitro. Upon transplantation into nude mice the cells have tumorigenic properties.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7946653 | PMC |
| http://dx.doi.org/10.1134/S1607672921010014 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Role of Aryl Hydrocarbon Receptor in Skin Homeostasis: Implications for Therapeutic Strategies in Skin Disorders.
Cell Biochem Funct
February 2025
Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, is extensively expressed in diverse human organs and plays a pivotal role in mediating the onset, progression, and severity of numerous diseases. Recent research has explored the substantial impact of AhR on skin homeostasis and related pathologies. As a multi-layered organ, the skin comprises multiple cell populations that express AhR.
View Article and Find Full Text PDFCDK1-loaded extracellular vesicles promote cell cycle to reverse impaired wound healing in diabetic obese mice.
Mol Ther
January 2025
Department of Surgery, University of California San Diego, La Jolla, CA, 92093, United States; Department of Dermatology, University of California San Diego, La Jolla, CA, 92093, United States. Electronic address:
Small extracellular vesicles (sEVs) mediate intercellular signaling to coordinate proliferation of cell types that promote re-epithelialization of skin following injury. Cyclin-dependent kinase 1 (CDK1) drives cell division and is a key regulator of entry to cell cycle. To understand the potential of sEV-mediated delivery of CDK1 to reverse impaired wound healing, we generated CDK1-loaded sEVs (CDK1-sEVs) and evaluated their ability to mediate cell proliferation, re-epithelialization and downstream signaling responses in the wound bed.
View Article and Find Full Text PDFZBP1-mediated PANoptosis is a crucial lethal form in diverse keratinocyte death modalities in UVB-induced skin injury.
Cell Death Dis
January 2025
Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing, 210042, Jiangsu, China.
UVB irradiation induces diverse modalities of regulatory cell death in keratinocytes. Recently, the pattern of coexistence of pyroptosis, apoptosis, and necroptosis has been termed PANoptosis; however, whether PANoptosis occurs in keratinocytes in UVB-induced skin injury remains unclear. We observed that the key molecules of GSDMD-mediated pyroptosis, apoptosis, and necroptosis, which are N-terminal GSDMD, cleaved caspase-3/PARP, and phosphorylated MLKL, respectively, were elevated in keratinocytes of UVB-challenged mice and human skin tissue.
View Article and Find Full Text PDFAnthracyclines disaggregate and restore mutant p63 function: a potential therapeutic approach for AEC syndrome.
Cell Death Discov
January 2025
Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA.
Ankyloblepharon-Ectodermal Defects-Cleft Lip/Palate (AEC) syndrome is a rare genetic disorder caused by mutations in the TP63 gene, which encodes a transcription factor essential for epidermal gene expression. A key feature of AEC syndrome is chronic skin erosion, for which no effective treatment currently exists. Our previous studies demonstrated that mutations associated with AEC syndrome lead to p63 protein misfolding and aggregation, exerting a dominant-negative effect.
View Article and Find Full Text PDFAutophagy-Enhancing Properties of Extracts in HaCaT Keratinocytes: Potential as an Anti-Photoaging Cosmetic Ingredient.
Molecules
January 2025
Graduate School of Biotechnology, Kyung Hee University, Yongin-si 17104, Republic of Korea.
The decline in autophagy disrupts homeostasis in skin cells, leading to oxidative stress, energy deficiency, and inflammation-all key contributors to skin photoaging. Consequently, activating autophagy has become a focal strategy for delaying skin photoaging. Natural plants are rich in functional molecules and widely used in the development of anti-photoaging cosmetics.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!