To directly compare the expression patterns of different proteins known to be altered during mouse skin carcinogenesis, serial sections of normal and hyperplastic skin and tumors from various stages of 7,12-dimethylbenz[a]anthracene-initiated, 12-O-tetradecanoylphorbol-13-acetate-promoted female SEN
Alteration of Egr-1 mRNA during multistage carcinogenesis in mouse skin
✍ Scribed by Penny K. Riggs; Okkyung Rho; John DiGiovanni
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 130 KB
- Volume
- 27
- Category
- Article
- ISSN
- 0899-1987
No coin nor oath required. For personal study only.
✦ Synopsis
Immediate early genes, including fos, jun, and early growth response-1 (Egr-1), are induced during cellular response to changes in extracellular environment. These immediate early genes are believed to mediate processes of cell growth and differentiation. In particular, Egr-1 is induced during mitogenic stimulation of a variety of cell types, including fibroblasts, B cells, and epithelial cells. In the present study, we examined Egr-1 gene expression during multistage carcinogenesis in mouse skin. After a single topical treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) to SENCAR mouse skin, Egr-1 mRNA was induced, and maximal induction was observed at 2 h in both epidermis and dermis. Induction of Egr-1 mRNA by TPA was inhibited by fluocinolone acetonide, a potent inhibitor of tumor promotion by TPA. Egr-1 mRNA was present in primary keratinocytes derived from adult SENCAR mice. The keratinocyte cultures were maintained in low Ca 2 medium, and Egr-1 mRNA levels became significantly elevated after the cultures were switched to high Ca 2 medium. Additionally, a large proportion of primary papillomas and carcinomas generated from SENCAR mice by standard initiation-promotion regimens exhibited elevated Egr-1 mRNA compared with normal epidermis. Taken together, these data suggest a possible role of Egr-1 during multistage carcinogenesis in mouse skin.
📜 SIMILAR VOLUMES
## Abstract Transforming growth factor (TGF)‐β1, whose gene is located on mouse chromosome 7, has been proposed to be involved in skin carcinogenesis. In the study presented here, we demonstrated that single topical treatments with different types of tumor promoters, i.e., the protein kinase C acti
Interleukin-1 receptor antagonist (IL-1Ra) is an endogenous inhibitor of interleukin-1. The expression of IL-1Ra and interleukin-1α (IL-1a) was measured in murine epidermis after treatment with tumor promoters and in tumor cell lines. A single treatment with three different tumor promoters (12-O-tet
The role of transforming growth factor-beta 1 (TGF-beta 1) in multisage carcinogenesis in mouse skin was assessed by studying its growth inhibitory effects on nontumorigenic and tumorigenic keratinocytes and by examining its mRNA expression in vitro and during epidermal hyperproliferation and multis
## Abstract An anti–tumor‐promoting effect of indomethacin and related nonsteroidal anti‐inflammatory drugs (NSAIDs) as well as the ability of the tumor promoter 12‐__O__‐tetradecanoylphorbol‐13‐acetate (TPA) to increase the level of prostaglandins in murine keratinocytes and mouse epidermis in viv
## Abstract Differentiation‐related gene‐1 (__Drg‐1__) has been identified as a gene whose expression is increased in several processes related to differentiation, but its function is currently unknown. In this report, we show that __Drg‐1__ was expressed in keratinocytes, this expression being rap