MCF7 cells

Induction ofmRNA for pS2 and secretion of cell-type-specific proteins. pS2 was measured in the culture medium of MCF7 cells with the ELSA-pS2 immunoradiometric assay (CIS Bio International, Gif-sur-Yvette, France). Cells were subcultured in 24-well plates for 144 h in 10% CDHuS. The culture medium was centrifuged at 1200g for 10 min to eliminate floating and detached cells. Results are expressed as ng of secreted protein per million cells. The relative-induced protein potency (RIPP) was calculated as 100 X the ratio between the dose of E2 and that of the chemical needed to produce maximal expression of cell-type-specific proteins (pS2). 

Fig. 7.3.1. Effect of estradiol on MCF7 cell proliferation. MCF7 cells were grown for 6 days in estrogen-depleted medium supplemented with 5% charcoal dextran-treated human serum (5% CDHuS) or with insulin (100 ng mP1) and transferrine (25 p,g ml-1) (ITDME). Estradiol was added to cultures at concentrations ranging from 0.1 pM to 1 nM. The maximal estrogenic response corresponded to 10 pM of estradiol and higher concentrations. Cell yields were six-fold (10 pM, 6.7 1.2) those of control. No proliferative response was observed in cells maintained in ITDME. Each point is the mean of three counts from four culture wells bars indicate SDs.

Fig. 7.3.2. Effect of estradiol and BP-5 on MCF7 cell proliferation and gene expression. MCF7 cells were grown in estrogen-depleted medium. Estradiol or BP-5 were added to cultures and cell number (proliferation), protein determination (PgR and pS2), gene expression (pS2 mRNA) and luciferase expression were estimated at the appropriate times, as indicated in the Methods Section.

In the E-Screen bioassay, LAS was not effective in promoting cell proliferation (Table 7.3.3). This compound was tested at concentrations of up to 100 pM with no evidence of cellular toxicity. The antiestrogenic effect of this compound was also measured but all samples tested were negative. Because it has been suggested that surfactants of the alkylbenzene sulfonate type are readily degradable and transformed into sulfophenyl carboxylates or SPCs, an important number of SPCs were assayed in the E-Screen test. These SPCs did not induce cell proliferation of MCF7 cells. 

Linear alcohols were studied using MCF7 cells in the proliferation assay and in the expression of estrogen-dependent genes (Table 7.3.4). The AS C12 i4, its ethoxylated derivative (ALFONIC 1214) and linear alcohols from nonanol to dodecanol increase cell proliferation in the E-Screen assay. This effect was seen at 10-100 xM concentrations and,... 

The same chemicals were also effective inductors of other markers of estrogenic action, such as PgR and pS2, in MCF7 cells. They increased... 

AG and APG were assayed in the E-Screen test for estrogenicity but were ineffective in inducing MCF7 cell proliferation. Table 7.3.3 shows the results of the proliferation test. 

Figure 6.1 Effects of various concentrations of HDAC inhibitors on acetylation of a-tubulin and histone in MCF7 human breast carcinoma cells. MCF7 cells were incubated for 5 h with various HDAC inhibitors at the indicated concentrations.

ChIP-on-chip data analysis based on estrogen receptor and RNAPolII enrichments in MCF7 cells [20]. 

Assay for reversal of MDR drug-resistant subline of breast cancer MCF7 cells the same method was used as in the case of mouse lymphoma, above. 

The comparison of the sensitivity of mouse lymphoma and human breast cancer MCF7 cell lines shows that the same human MDR1 gene-encoded P-gp... 

The chlorinated pesticides DDT and chlordecone are known to generate deleterious reproductive effects. In a bioassay of these and other chlorinated pesticides on cultured human breast estrogen-sensitive MCF7 cells, it was shown that dieldrin, toxaphene, and endosulfan have estrogenic properties comparable to those of DDT and chlordecone. When tested together, the mixture of the three pesticides induced estrogenic responses... 

Coezy E, Borgna JL, Rochefort H. Tamoxifen and metabolites in MCF7 cells correlation between binding to estrogen receptor and inhibition of cell growth. Cancer Res 1982 42(l) 317-23. 

---