Estrogenic effect of phenol red in MCF-7 cells is achieved through activation of estrogen receptor by interacting with a site distinct from the steroid binding site

Rajendran, K. G.; Lopez, T.; Parikh, Indu

doi:10.1016/0006-291x(87)91474-4

Cited by 38 publications

(17 citation statements)

References 14 publications

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“…Effects occurred with 17p-estradiol in concentrations considered to be available to cells in vivo under physiological conditions (18). Moreover, the effect of 17,3-estradiol on bone-forming cells appears spe- (20,21) and to bind to the estradiol receptor, also stimulated osteoblastlike cell proliferation. (iv) Tamoxifen (1 ,uM) abolished the phenol red-induced osteoblast-like cell stimulation, as expected for estradiol-sensitive cells (21,22).…”

Section: Discussionmentioning

confidence: 99%

“…Among the best-characterized estrogen actions are those on the mammary gland [including carcinoma cell lines (19)(20)(21)] and on the uterus. It has recently been shown that estradiol administered in vivo to rats enhanced proal(I) collagen gene expression in the uterus (28).…”

Section: Discussionmentioning

confidence: 99%

“…For the determination of collagen synthesis, culture dishes (35 mm) were pulsed with 3 gCi/ml [5-3H]proline (20 Ci/mmol; 1 Ci = 37 GBq; Amersham) in the presence of ascorbic acid at 50 ,tg/ml for the last 2 days of culture. After labeling, 1 ml of phosphatebuffered saline containing 6.3 mM N-ethylmaleimide/2 mM phenylmethylsulfonyl fluoride/25 mM EDTA, pH 7.2 (PBS+) was added to the medium.…”

Section: Methodsmentioning

confidence: 99%

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Enhanced osteoblast proliferation and collagen gene expression by estradiol.

Ernst

Schmid

Froesch

1988

Proc. Natl. Acad. Sci. U.S.A.

194

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Estrogens play a crucial role in the development of postmenopausal osteoporosis. However, the mechanism by which estrogens exert their effects on bone is unknown. Postmenopausal osteoporosis is delayed or prevented by substitution with estrogens (1-3). The mechanism by which estrogens exert their effects on bone is unknown, although it is thought that, at least in part, they may inhibit bone resorption (3). Estrogens may affect bone cells directly or indirectly via systemic or local factors. In the adult, continuous bone formation and resorption (remodeling) are highly regulated to permit bone to exert its major functions, mechanical support and mineral homeostasis (4). Estrogens may either affect the concerted process of bone remodeling, or transmit or modify signals selectively inducing bone formation or bone resorption. These signals control proliferation, differentiation, and other functions of highly specialized cell types, osteoclasts and osteoblasts. The latter are responsible for bone formation and at the same time crucially regulate bone-resorbing osteoclasts (5). Despite the well-documented effects of estrogens on bone in vivo (1-3, 6), finding estrogen receptors in bone has been difficult (7, 8).To examine whether 17f-estradiol directly affects boneforming cells, we used rat osteoblast-like cells in vitro under strictly serum-free conditions as a model (9). In this culture system calvaria cells express characteristics of osteoblastlike cells, such as alkaline phosphatase activity and responsiveness to parathyroid hormone (in terms of cAMP), to a higher degree than identically prepared cells grown under conventional culture conditions. We found in long-term cultures that 17p8-estradiol (i) stimulates cell proliferation in a dose-dependent fashion and (ii) increases steady-state levels of mRNA encoding the al chain of type I procollagen. Thus, estrogens stimulate bone formation by a direct action on osteoblasts.MATERIALS AND METHODS Cell Culture. Calvaria of newborn rats (ZUR:SIV, formerly Sprague-Dawley) were sequentially digested with bacterial collagenase, and the released osteoblast-like cells were inoculated in serum-free viscous medium as described elsewhere (9). In brief, single cells were seeded at about 1.3 x 105 cells per culture dish (Falcon, 35 mm in diameter) in 1 ml of serum-free, viscous minimal essential medium alpha/ F-12 medium (1:1 mixture, both from GIBCO, without phenol red) containing 0.25% delipidated bovine serum albumin (Serva) and 0.8% methylcellulose (MeC) (Serva). Osteoblast-like cells remain selectively as cuboidal cells in MeC medium, sediment to the bottom of the dish, and are anchored by extracellular matrix domains, mainly type I collagen (9).17,3-Estradiol (Sigma), the biologically inactive stereoisomer 17a-estradiol (Sigma), and the antiestrogen transtamoxifen (Sigma) were added at the beginning of the culture period, which lasted for 19-21 days (370C, humidified atmosphere of 90% N2/5% C02/5% 02).Growth Curves. In MeC medium, osteoblast-like cells proliferate ...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Enhanced osteoblast proliferation and collagen gene expression by estradiol.

Ernst

Schmid

Froesch

1988

Proc. Natl. Acad. Sci. U.S.A.

194

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“…Cells were cultured in Minimum Essential Medium Eagle's and Dulbecco's Modified Eagle Medium supplemented with 10 % foetal bovine serum and penicillinstreptomycin at 37°C in a 5 % CO 2 humidified atmosphere MCF-7 cells were cultured in estrogen depleted medium opti-MEM and estrogen stimulation was performed by adding phenol red at a concentration of 50 μM, as at these concentrations phenol red causes estrogenic effect in MCF-7 cells through activation of cytoplasmic receptor by interacting at a site distinct from the steroid-binding site. [16].…”

Section: Cell Culturementioning

confidence: 95%

Silencing of ZRF1 impedes survival of estrogen receptor positive MCF-7 cells and potentiates the effect of curcumin

et al. 2016

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The role and clinical implication of ZRF1 in breast cancer are poorly understood. So this study is aimed to explore the role of ZRF1 in breast cancer progression. With this context, we first assessed its expression pattern in FFPE primary and metastasis breast tissue samples as well as from publicly available databases. Moreover, we also explored the survival status of patients from the publicly available database and interestingly discover that high expression of ZRF1 decreases the survival of estrogen-positive breast cancer patients more than estrogen-negative status patients. In the perspective of this, we evaluated the role ZRF1 in MCF-7 breast cancer cells and found that it's silencing by knockdown results in decreased cell proliferation as well as cell viability. Results also show that expression of ZRF1 is down regulated in the presence of estrogen-depleted conditions but independent of RAS/MEK as well as AKT axes. Moreover, the decrease in viability of MCF-7 cells was accompanied by induction of apoptosis and DNA damage, well-marked with upregulation of cleaved PARP and downregulation of BCL2 and H2AUbK119 levels. Furthermore, we also explored that knockdown of ZRF1 sensitises the effect of curcumin, observed with decrease in cell viability and dropping of IC50 value from 25 to 15 μM. This investigation thus shed a new light on the role on ZRF1 in breast cancer cells and hence can be exploited to design better therapeutic intervention.

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“…Because several studies have shown that the presence of phenol red in culture or perifusion media can act as a weak oestrogen (Hubert, Vincent & Labrie, 1986;Hofland, van Koetsveld, Koper et al 1987;Rajendran, Lopez & Parikh, 1987), the earlier studies (Kerdelhué, Valens & Langlois, 1978 ;Kerdelhué, Battmann, Parnet et al 1987) have been repeated in the absence of phenol red.…”

Section: Introductionmentioning

confidence: 95%

In-vivo inhibition of the preovulatory LH surge by substance P and in-vitro modulation of gonadotrophin-releasing hormone-induced LH release by substance P, oestradiol and progesterone in the female rat

Battmann

Parsadaniantz²,

Jeanjean³

et al. 1991

Journal of Endocrinology

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The effects of substance P (SP) on the preovulatory surge of LH and on the inhibitory and stimulatory effects of oestradiol-17 beta and progesterone on gonadotrophin-releasing hormone (GnRH)-induced LH release were investigated in vivo and in vitro in the rat. A single s.c. injection of 100 micrograms SP at 12.00 h on the day of pro-oestrus significantly decreased the preovulatory surge of LH. In vitro, the inhibitory effect of oestradiol-17 beta on GnRH-induced LH release was not modified by treatment with SP. The stimulatory effect of progesterone on GnRH-induced LH release was reduced by treatment with SP. It is concluded that SP may play a modulatory role in the neuroendocrine control of the preovulatory LH surge.

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Estrogenic effect of phenol red in MCF-7 cells is achieved through activation of estrogen receptor by interacting with a site distinct from the steroid binding site

Cited by 38 publications

References 14 publications

Enhanced osteoblast proliferation and collagen gene expression by estradiol.

Enhanced osteoblast proliferation and collagen gene expression by estradiol.

Silencing of ZRF1 impedes survival of estrogen receptor positive MCF-7 cells and potentiates the effect of curcumin

In-vivo inhibition of the preovulatory LH surge by substance P and in-vitro modulation of gonadotrophin-releasing hormone-induced LH release by substance P, oestradiol and progesterone in the female rat

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