The role of two important tumour suppressor genes, p16 and p53, was evaluated in cartilaginous tumour tissues. Genomic DNA from 22 chondrosarcomas, 5 benign chondroid tumours, 1 sample of reactive proliferative cartilage and 2 samples of normal cartilage were analysed using polymerase chain reaction
Possible involvement of p21 but not of p16 or p53 in keratinocyte senescence
β Scribed by Koji Sayama; Yuji Shirakata; Kazushige Midorikawa; Yasushi Hanakawa; Koji Hashimoto
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 141 KB
- Volume
- 179
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
β¦ Synopsis
It has been reported that p21, p53, and p16 affect the cell cycle and cell senescence. However, their roles in keratinocyte senescence are not clear. We established primary keratinocyte strains from 15 donors and maintained them until replicative senescence; their population doublings ranged from 5.7-45.2. These strains were classified based on their population doublings as short (5.7-10.4), intermediate (13.9 -17.4), and long (21.5-45.2). To investigate the roles of p21, p53, and p16 in the cellular senescence of the cultured keratinocytes, we quantitatively analyzed p21, p53, and p16 levels of keratinocyte strains with different life spans by Western blot with FluoroImager. p21 levels increased in the senescent phase but not in the nonsenescent phase in all of the short, intermediate, and long life-span strains. Northern blot analysis also revealed induction of p21 mRNA was similar to that of p21 protein levels. There were no apparent differences in p53 levels between senescent and nonsenescent cells. The short life-span strains exhibited a significant increase in p16 levels in the senescent phase (eighth or tenth passage). However, in two long life-span strains, p16 levels were increased in the nonsenescent phase (eighth passage) but then declined as the cells reached senescence (twenty-seventh passage). Therefore, induction of p16 appeared not to be associated with senescence in long life-span strains. In conclusion, p21 but not p16 or p53 may play roles in keratinocyte senescence.
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