The DOI matches its Crossref record; 123 of the 123 references it cites were found in a registry or an index.
Sex steroidal regulation of uterine leiomyoma growth and apoptosis
Abstract
Uterine leiomyomas develop during the reproductive years and regress after menopause, indicating ovarian steroid-dependent growth potential. Although the clinical and biochemical observations have traditionally supported an important role for estrogen in the promotion of leiomyoma growth, there is also increasing evidence to suggest the involvement of progesterone in the pathogenesis of leiomyoma. In this review, much attention has been paid to characterizing the molecular mechanisms of sex steroidal regulation of leiomyoma growth and apoptosis by evaluating the effects of sex steroids on the expression of growth factors and apoptosis-related factors. The effects of GnRH agonist on the expression of these factors in leiomyoma are also described. 17beta-Estradiol up-regulates epidermal growth factor (EGF) receptor, but down-regulates p53 protein in leiomyoma cells, whereas progesterone augments EGF and Bcl-2 protein, but inhibits insulin-like growth factor (IGF-I) and tumour necrosis factor (TNFalpha). Since it is now evident that EGF and IGF-I act as local factors which stimulate leiomyoma growth, these findings suggest that progesterone may have dual actions, stimulatory and inhibitory, on leiomyoma cell growth and survival, depending on the local growth factor conditions around each leiomyoma. This may explain why the size of uterine leiomyomas during the use of levonorgestrel-releasing intrauterine system (LNG-IUS) increases in some but decreases in other instances. This may also explain why the size of leiomyomas during pregnancy does not increase despite the overwhelming increase in circulating concentrations of sex steroid hormones. Moreover, there is further evidence to suggest that the interactions between estrogen receptors and progesterone receptors may be involved in the modulation of gene transcription activity in leiomyoma. This review demonstrates that leiomyoma growth is integrally regulated by the complex cross-talk between sex steroid hormones and growth factors.
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Cites
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“Since p53 is a tumour suppressor gene that directly regulates the growth of tumours by inhibiting tumour cell growth or promoting cell death (Kastan et al., 1992; Oltvai et al., 1993; Miyashita et al., 1994, 1995), E 2 may stimulate leiomyoma growth in part by decreasing the p53 protein levels and…”
BackgroundInfluentialMutations in the p53 gene occur in diverse human tumour types
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Cited by
Progesterone action in endometrial cancer, endometriosis, uterine fibroids, and breast cancer
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Metadata
- Authors
- Maruo, T.
- Venue
- Human Reproduction Update
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-05-01
- Volume
- 10
- Issue
- 3
- Pages
- 207-220
- ISSN
- 1355-4786 (ISSN-L)
- 1460-2369
- OpenAlex
- W2110117792
- Cited by
- 294
- References
- 123
- FWCI
- 13.48
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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