The interaction of cytokines in regulating oestradiol 17β-hydroxysteroid dehydrogenase activity in MCF-7 cells
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Role of hydroxysteroid (17beta)dehydrogenase type 1 in reproductive tissues and hormone-dependent diseases
2019, Molecular and Cellular EndocrinologyCitation Excerpt :Similarly, many factors that stimulate breast cancer proliferation, including IL1 and TNFA, also upregulate HSD17B1 expression in breast cancer cells (Nagasaki et al., 2009) (Table 4). Furthermore, various other cytokines and growth factors, such as IGF1 and 2, IL6 and IL1B, typically produced by inflammatory cells and adipocytes, have been shown to induce E1 to E2 activity in breast cancer cells (Adams et al., 1991; Singh and Reed, 1991; Speirs et al., 1993; Duncan et al., 1994; Duncan and Reed, 1995), suggesting that the inflammation process in breast tumors enhances the tumor-acquired estrogen biosynthesis ability. Furthermore, E1 to E2 activity was increased in breast fibroadenomas in the luteal phase compared to follicular phase and in patients using oral progestins (Fournier et al., 1982), suggesting a role for progestins in the regulation of HSD17B1, an action also shown in breast cancer cells in vitro (Poutanen et al., 1990).
HSD17B1 expression enhances estrogen signaling stimulated by the low active estrone, evidenced by an estrogen responsive element-driven reporter gene in vivo
2015, Chemico-Biological InteractionsCitation Excerpt :Similarly to P450 aromatase (CYP19A1), the expression of HSD17B1 is related to follicular differentiation and positively correlates with the follicular E2 concentration. Granulosa cells of developing and luteinizing follicles express HSD17B1 [27], and various factors that enable the antral-to-preovulatory transition of follicles, including FSH, LH, GH, IGF1, EGF, TGFα, FGF2 and IL1B [28], also up-regulate HSD17B1 expression [29–34]. Of ovarian cancers, the vast majority (80–90%) is derived from the ovarian surface epithelium, and epidemiological evidence suggests that steroid hormones, especially estrogens and progestins, are implicated in ovarian carcinogenesis [35].
Estradiol regulates Tumor Necrosis Factor-α expression and secretion in Estrogen Receptor positive breast cancer cells
2014, Molecular and Cellular EndocrinologyCitation Excerpt :TNFα maintains these surrounding fibroblasts in an undifferentiated state, thus maintaining their estrogen-producing capacity (Zhang et al., 1996). TNFα is also critical in regulating the expression and activity of key enzymes involved in the estrogen biosynthesis pathway, therefore increases in TNFα signalling to surrounding fibroblasts results in a net increase in estrogen levels within the breast tumor microenvironment (Purohit et al., 1996; Duncan et al., 1994; Zhao et al., 1997). In turn, we have shown that estrogen may then upregulate transcript and secreted levels of TNFα in ER+ breast tumor cells.
Endometriosis as a model for inflammation-hormone interactions in ovarian and breast cancers
2006, European Journal of CancerThe regulation and inhibition of 17β-hydroxysteroid dehydrogenase in breast cancer
2006, Molecular and Cellular Endocrinology