Effect of antiestrogens and aromatase inhibitor on basal growth of the human breast cancer cell line MCF-7 in serum-free medium

Jensen, Jens Fog; Kitlen, Jason W.; Briand, Per; Labrie, Fernand; Lykkesfeldt, Annè E.

doi:10.1016/s0960-0760(03)00068-2

Cited by 23 publications

(24 citation statements)

References 43 publications

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“…Cells were harvested from sub-confluent flasks using RIPA buffer (containing 1 mM dithiothreitol, 1 mM sodium fluoride and a protease inhibitor cocktail (Sigma)) as previously described (Jensen et al, 2003). Snap frozen tissue pieces of approximately 30 mg were lysed in the same buffer using an UltraTurrax dispersing tool.…”

Section: Western Blot and Antibodiesmentioning

confidence: 99%

Loss of tumourigenicity of stably ERβ-transfected MCF-7 breast cancer cells

Behrens¹,

Gill²,

Fichtner³

2007

Molecular and Cellular Endocrinology

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Section: Western Blot and Antibodiesmentioning

confidence: 99%

Loss of tumourigenicity of stably ERβ-transfected MCF-7 breast cancer cells

Behrens¹,

Gill²,

Fichtner³

2007

Molecular and Cellular Endocrinology

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“…On the other hand, raloxifene shows protection against vertebral fractures similar to bisphosphonates; although, however, no significant effect has been observed on nonvertebral fractures. Acolbifene (ACOL) (EM-652.HCl), a third-generation SERM, a prodrug of EM-652, has been used to prevent the development of and to treat established mammary tumors in animal models [27,36,64,66]. While hormone therapy was previously believed to be only cytostatic, it was observed, for the first time with an hormonal agent, that ACOL caused the disappearance of 61 % of human breast cancer tumors in nude mice, thus demonstrating cytotoxic activity [84].…”

Section: Introductionmentioning

confidence: 99%

Specific transcriptional response of four blockers of estrogen receptors on estradiol-modulated genes in the mouse mammary gland

Calvo

Luu‐The

Belleau

et al. 2012

Breast Cancer Res Treat

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Novel agents for the endocrine therapy of breast cancer are needed, especially in order to take advantage of the multiple consecutive responses observed in metastatic progressing breast cancer following previous hormone therapy, thus delaying the use of cytotoxic chemotherapy with its frequent poor tolerance and serious side effects. Acolbifene (ACOL) is a novel and unique antiestrogen which represents a unique opportunity to achieve the most potent and specific blockade of estrogen action in the mammary gland and uterus while exerting estrogen-like beneficial effects in other tissues, especially the bones. To better understand the specificity of action of ACOL, we have used Affymetrix GeneChips containing 45,000 probe sets to analyze 34,000 genes to determine the specificity of this compound compared to the pure antiestrogen fulvestrant, as well as to the mixed antagonists/agonists tamoxifen and raloxifene to block the effect of estradiol (E(2)) and to induce effects of their own on the genomic profile in the mouse mammary gland. The genes modulated by E(2) were those identified in two separate experiments and validated by quantitative real-time PCR (qPCR). Three hours after the single subcutaneous injection of E(2) (0.05 μg), the simultaneous administration of ACOL, fulvestrant, tamoxifen, and raloxifene blocked by 98, 61, 43, and 92 % the number of E(2)-upregulated genes, respectively. On the other hand, 70, 10, 25, and 55 % of the genes down-regulated by E(2) were blocked by the same compounds. Of the 128 genes modulated by E(2), 49 are associated with tumorigenesis while 22 are known to be associated with breast cancer. When used alone, ACOL modulated the smallest number of genes also influenced by E(2), namely 4 %, thus possibly explaining potential utilities of this compound in breast cancer prevention and therapy.

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“…In order to investigate this hypothesis, prenylated xanthones were studied in steroid-free medium (SFM), an in vitro environment that mimics the effects of several antitumor agents in therapy (Jensen et al, 2003). 3,4-Dihydro-12-hydroxy-2,2-dimethyl-2H,6H-pyrano[3,2-b]xanthen-6-one (4) along with two linear analogs (5, 6) of 3,4-dihydroxyxanth-9-one (3) were selected for analysis of their inhibitory effect on the growth of human tumor cell lines.…”

Section: Introductionmentioning

confidence: 99%

Prenylated xanthones: antiproliferative effects and enhancement of the growth inhibitory action of 4-hydroxytamoxifen in estrogen receptor-positive breast cancer cell line

et al. 2011

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The effects of three prenylated xanthones on the in vitro growth of estrogen-dependent ER (?) MCF-7 (breast), estrogen-independent ER (-) MDA-MB-231 cells (breast), and NCI-H460 (non-small cell lung) were investigated in a complete and/or steroid-free medium. 3,4-Dihydro-12-hydroxy-2,2-dimethyl-2H,6H-pyrano[3,2-b]xanthen-6-one (4), the most potent against the ER(?) MCF-7 cell line (GI 50 = 5 lM), showed an enhancement in the anti-estrogenic effect of 4-hydroxytamoxifen in this ER(?) cell line.

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Effect of antiestrogens and aromatase inhibitor on basal growth of the human breast cancer cell line MCF-7 in serum-free medium

Cited by 23 publications

References 43 publications

Loss of tumourigenicity of stably ERβ-transfected MCF-7 breast cancer cells

Loss of tumourigenicity of stably ERβ-transfected MCF-7 breast cancer cells

Specific transcriptional response of four blockers of estrogen receptors on estradiol-modulated genes in the mouse mammary gland

Prenylated xanthones: antiproliferative effects and enhancement of the growth inhibitory action of 4-hydroxytamoxifen in estrogen receptor-positive breast cancer cell line

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