Inhibition of growth‐factor‐activated proliferation by anti‐estrogens and effects on early gene expression of mcf‐7 cells

Wosikowski, Katja; Küng, Willy; Hasmann, Max; Löser, R.; Eppenberger, Urs

doi:10.1002/ijc.2910530220

Cited by 50 publications

(21 citation statements)

References 21 publications

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“…As reported previously (31), the ICI antiestrogen inhibited EGF-induced mitogenesis. Furthermore, EGF-stimulated DNA synthesis was inhibited by the same compounds to virtually the same degree as was seen with E 2 treatment ( Fig.…”

Section: Cytoplasmic Signaling Inhibitors Prevent Estrogen-inducedsupporting

confidence: 86%

Characterization of the Breast Cancer Susceptibility Gene BRCA2

Lobenhofar¹,

Marks²

2000

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Section: Cytoplasmic Signaling Inhibitors Prevent Estrogen-inducedsupporting

confidence: 86%

Characterization of the Breast Cancer Susceptibility Gene BRCA2

Lobenhofar¹,

Marks²

2000

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“…Tamoxifen, even if it actually competes with estrogens for the binding to estrogen receptor, cannot be considered as a pure antiestrogen since tamoxifen-estrogen-receptor complexes can activate the estrogen response element of some genes [37]. Some effects could also result from the association of these antiestrogens with other binding sites such as the antiestrogen binding site [38].…”

Section: Discussionmentioning

confidence: 99%

Intracellular Levels and Secretion of Insulin‐Like‐Growth‐Factor‐Binding Proteins in MCF‐7/6, MCF‐7/AZ and MDA‐MB‐231 Breast Cancer Cells

Dubois

Couissi

Schonne

et al. 1995

European Journal of Biochemistry

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The synthesis and secretion of insulin-like growth factor binding proteins (IGFBPs) were studied in MDA-MB-23 1 (estrogen-receptor-negative), MCF-7/6 (estrogen-receptor-positive, invasive) and in MCF-7/AZ (estrogen-receptor-positive, non-invasive) human breast carcinoma cell lines. Cells were grown or maintained in a chemically defined medium. Under these conditions, we found different patterns of IGFBPs in the three cell types. MDA-MB-231 cells secrete most of the IGFBPs they produce whereas MCF-7/6 and MCF-7/AZ cells maintain a high intracellular level. In MDA-MB-231 cells, the major IGFBP is IGFBP-4 which is the minor form in MCF-7/6 and MCF-7/AZ cells. IGFBP-2 and IGFBP-5 are predominant in MCF-7/6 cells while MCF-7/AZ cells produce far less IGFBPs and do not contain detectable amounts of 29-32-kDa forms (IGFBP-5). In MCF-7/6 cells, estradiol-17/? specifically decreases both the intracellular content and secretion of IGFBP-2 and IGFBP-5. Estrogen regulation of IGFBPs cell content and secretion was found to be tamoxifen-resistant, and only slightly antagonized by ICI 182,780, a pure antiestrogen. The function of these regulations relative to the invasive phenotype and proliferation has now to be determined.

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“…The Crystal Violet assay as described by Wosikowski et al [9] was used to determine cell viability. Cells were seeded at approximately 10,000 cells per well in 48-well plates and allowed to adhere overnight.…”

Section: Crystal Violet Assay For Viable Cell Numbermentioning

confidence: 99%

Autophagic cell death, polyploidy and senescence induced in breast tumor cells by the substituted pyrrole JG-03-14, a novel microtubule poison

Arthur

Gupton

Kellogg

et al. 2007

Biochemical Pharmacology

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JG-03-14, a substituted pyrrole that inhibits microtubule polymerization, was screened against MCF-7 (p53 wild type), MDA-MB 231 (p53 mutant), MCF-7/caspase 3 and MCF-7/ADR (multidrug resistant) breast tumor cell lines. Cell viability and growth inhibition were assessed by the crystal violet dye assay. Apoptosis was evaluated by the TUNEL assay, cell cycle distribution by flow cytometry, autophagy by acridine orange staining of vesicle formation, and senescence based on β-galactosidase staining and cell morphology. Our studies indicate that exposure to JG-03-14, at a concentration of 500 nM, induces time dependent cell death in the MCF-7 and MDA-MB 231 cell lines. In MCF-7 cells, a residual surviving cell population was found to be senescent; in contrast, there was no surviving senescent population in treated MDA-MB 231 cells. No proliferative recovery was detected over a period of 15 days post-treatment in either cell line. Both the TUNEL assay and FLOW cytometry indicated a relatively limited degree of apoptosis (< 10%) in response to drug treatment in MCF-7 cells with more extensive apoptosis (but < 20%) in MDA-MB231 cells; acidic vacuole formation indicative of autophagic cell death was relatively extensive in both MCF-7 and MDA-MB231 cells. In addition, JG-03-14 induced the formation of a large hyperdiploid cell population in MDA-MB231 cells. JG-03-14 also demonstrated pronounced anti-proliferative activity in MCF-7/caspase 3 cells and in the MCF-7/ADR cell line. The observation that JG-03-14 promotes autophagic cell death and also retains activity in tumor cells expressing the multidrug resistance pump indicates that novel microtubule poisons of the substituted pyrroles class may hold promise in the treatment of breast cancer.

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Inhibition of growth‐factor‐activated proliferation by anti‐estrogens and effects on early gene expression of mcf‐7 cells

Cited by 50 publications

References 21 publications

Characterization of the Breast Cancer Susceptibility Gene BRCA2

Characterization of the Breast Cancer Susceptibility Gene BRCA2

Intracellular Levels and Secretion of Insulin‐Like‐Growth‐Factor‐Binding Proteins in MCF‐7/6, MCF‐7/AZ and MDA‐MB‐231 Breast Cancer Cells

Autophagic cell death, polyploidy and senescence induced in breast tumor cells by the substituted pyrrole JG-03-14, a novel microtubule poison

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