Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA339617 | ENA |
REPOSITORIES: ENA
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Project description:RON WT and RON KO at 5, 6, 7 week virgin mammary glands In the study, we demonstrated that RON regulates mammary gland branching morphogenesis in pubertal development associated with changes in gene expression. Keywords: Pubertal mammary glands In the study, we hybridized RNA from 5, 6, 7 week old virgin female RON WT and KO mammary glands to Affymetrix GeneChip Mouse Genome 430 2.0 Array
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Project description:MicroRNAs are widely expressed in the normal pubertal mammary gland and orchestrate mammary gland development by regulating cell proliferation, differentiation, apoptosis, and metabolism. Although human Growth hormone(hGH) plays fundamental roles in normal mammary gland development and elevated autocrine hGH levels have been documented to contribute to breast cancer, whether hGH should influence the expression pattern and the functional roles of miRNAs in this context remain unknown.This study explores the effects of autocrine hGH on microRNA expression in MCF7 cell.
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Project description:Perinatal exposure to bisphenol A (BPA) has been shown to cause aberrant mammary gland morphogenesis and mammary neoplastic transformation. Yet, the underlying mechanism is poorly understood. We tested the hypothesis that mammary glands exposed to BPA during a susceptible window may lead to its susceptibility to tumorigenesis through a stem-cell mediated mechanism. We exposed 21-day-old Balb/c mice to BPA by gavage (25 µg/kg/day) during puberty for 3 weeks, and a subset of animals were further challenged with one oral dose (30 mg/kg) of 7,12-dimethylbenz[a]anthracene (DMBA) at 2 months of age. Primary mammary cells were isolated at 6 weeks, and 2 and 4 months of age for mammary stem cell (MaSC) quantification and function analysis. Pubertal exposure to the low-dose BPA increased lateral branches and hyperplasia in adult mammary glands and caused an acute increase of MaSC in 6-week-old glands and a delayed increase of luminal progenitors in 4-month-old adult gland. Most importantly, pubertal BPA exposure altered the function of MaSC from different age groups, causing pre-neoplastic lesions in their regenerated glands similar to those induced by DMBA exposure, which indicates that MaSCs are susceptible to BPA-induced transformation. Deep sequencing analysis on MaSC-enriched mammospheres identified a set of aberrantly expressed genes associated with pre-neoplastic lesions in human breast cancer patients. Thus, our study for the first time shows that pubertal BPA exposure altered MaSC gene expression and function such that they induced early neoplastic transformation.
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