Dataset Information

Insulin and IGF-1, but not 17?-estradiol, alter the subcellular localization of MIER1? in MCF7 breast carcinoma cells.

ABSTRACT: MIER1? is a transcriptional regulator that interacts with estrogen receptor ? and inhibits estrogen-stimulated growth of breast carcinoma cells. Interestingly, analysis of MIER1? subcellular localization in breast samples revealed a stepwise shift from the nucleus to the cytoplasm during progression to invasive carcinoma. Previously, we demonstrated that MIER1? is nuclear in MCF7 cells yet it does not contain a nuclear localization signal. Instead MIER1? is targeted to the nucleus through interaction and co-transport with HDAC 1 and 2.In this study, we demonstrate that treatment of MCF7 breast carcinoma cells with either insulin or insulin-like growth factor affects the subcellular localization of MIER1?. Both factors reduce the percentage of cells with nuclear MIER1? from 81 and 89 to 41 and 56%, respectively. Treatment with 17?-estradiol, on the other hand, had no effect and MIER1? remained nuclear.Our data demonstrate that insulin and IGF-1 can contribute to loss of nuclear MIER1? in the MCF7 breast carcinoma cell line.

SUBMITTER: Li S

PROVIDER: S-EPMC4539687 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature

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Insulin and IGF-1, but not 17β-estradiol, alter the subcellular localization of MIER1α in MCF7 breast carcinoma cells.

Li Shengnan S Paterno Gary D GD Gillespie Laura L LL

BMC research notes 20150818

<h4>Background</h4>MIER1α is a transcriptional regulator that interacts with estrogen receptor α and inhibits estrogen-stimulated growth of breast carcinoma cells. Interestingly, analysis of MIER1α subcellular localization in breast samples revealed a stepwise shift from the nucleus to the cytoplasm during progression to invasive carcinoma. Previously, we demonstrated that MIER1α is nuclear in MCF7 cells yet it does not contain a nuclear localization signal. Instead MIER1α is targeted to the nuc ...[more]

PMID: 26281834

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Project description:Breast cancer (BC) is a leading cause of cancer deaths in women in less developed countries and the second leading cause of cancer death in women in the U.S. In this study, we report the inhibition of E2-mediated mammary tumorigenesis by Cuminum cyminum (cumin) administered via the diet as cumin powder, as well as dried ethanolic extract. Groups of female ACI rats were given either an AIN-93M diet or a diet supplemented with cumin powder (5% and 7.5%, w/w) or dried ethanolic cumin extract (1%, w/w), and then challenged with subcutaneous E2 silastic implants (1.2 cm; 9 mg). The first appearance of a palpable mammary tumor was significantly delayed by both the cumin powder and extract. At the end of the study, the tumor incidence was 96% in the control group, whereas only 55% and 45% animals had palpable tumors in the cumin powder and extract groups, respectively. Significant reductions in tumor volume (660 ± 122 vs. 138 ± 49 and 75 ± 46 mm3) and tumor multiplicity (4.21 ± 0.43 vs. 1.16 ± 0.26 and 0.9 ± 0.29 tumors/animal) were also observed by the cumin powder and cumin extract groups, respectively. The cumin powder diet intervention dose- and time-dependently offset E2-related pituitary growth, and reduced the levels of circulating prolactin and the levels of PCNA in the mammary tissues. Mechanistically, the cumin powder diet resulted in a significant reversal of E2-associated modulation in ERα, CYP1A1 and CYP1B1. Further, the cumin powder diet reversed the expression levels of miRNAs (miR-182, miR-375, miR-127 and miR-206) that were highly modulated by E2 treatment. We analyzed the composition of the extract by GC/MS and established cymene and cuminaldehyde as major components, and further detected no signs of gross or systemic toxicity. Thus, cumin bioactives can significantly delay and prevent E2-mediated mammary tumorigenesis in a safe and effective manner, and warrant continued efforts to develop these clinically translatable spice bioactives as chemopreventives and therapeutics against BC.

Dataset Information

Insulin and IGF-1, but not 17?-estradiol, alter the subcellular localization of MIER1? in MCF7 breast carcinoma cells.

Publications

Insulin and IGF-1, but not 17β-estradiol, alter the subcellular localization of MIER1α in MCF7 breast carcinoma cells.

Similar Datasets

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