Effect of low dose bisphenol A on the early differentiation of human embryonic stem cells into mammary epithelial cells

Liu, Yang; Luo, Liaofu; Ji, Weidong; Gong, Chunmei; Wu, Desheng; Huang, Haiyan; Qingcheng, Liu; Xia, Bo; Hu, Gonghua; Zhang, Wenjuan; Zhang, Qian; Liu, Jing; Zhang, Wenchang; Zhuang, Zhixiong

doi:10.1016/j.toxlet.2013.01.026

Cited by 46 publications

(30 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Human embryonic stem cells (hESCs) isolated from the inner cell mass of blastocysts are one type of stem cells 151. A recent study showed that BPA affected the early differentiation of hESCs into mammary epithelial cells at doses as low as 1 nM 47. The increased levels of pluripotent molecular markers (Nanog, Oct4) and decreased levels of the marker of mammary epithelial cells (E‐cadherin) accounted for the adverse effects of BPA on hESC differentiation, promoting the cancerous state of mammary epithelial cells.…”

Section: Mechanisms Underlying Bpa‐stimulated Carcinogenic Effectsmentioning

confidence: 99%

“…BPA, one of the most ubiquitous and thoroughly studied EDCs, is also weakly estrogenic and there has been concern regarding the role BPA may play in the development of breast cancer over years 44, 45, 46. Epidemiological studies have linked BPA exposure to breast cancer‐related factors 47, 48. Many in vivo and in vitro studies have reported that exposure to BPA leads to mammary neoplastic lesions and malignant tumors 7, 45, 49.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

2016

View full text Add to dashboard Cite

Breast cancer is the fifth most common cause of cancer death in the world and the second most common fatal cancer in women. Epidemiological studies and clinical data have indicated that hormones, including estrogen, progesterone, and prolactin, play important roles in the initiation and progression of breast cancer. Bisphenol A (BPA) is one of the most commonly used and thoroughly studied endocrine disruptors. It can be released from consumer products and deposited in the environment, thus creating potential for human exposure through oral, inhaled, and dermal routes. Some recent reviews have summarized the known mechanisms of endocrine disruptions by BPA in human diseases, including obesity, reproductive disorders, and birth defects. However, large knowledge gaps still exist on the roles BPA may play in cancer initiation and development. Evidence from animal and in vitro studies has suggested an association between increased incidence of breast cancer and BPA exposure at doses below the safe reference doses that are the most environmentally relevant. Most current studies have paid little attention to the cancer‐promoting properties of BPA at low doses. In this review, recent findings on the carcinogenic effects of low‐dose BPA on breast cancer and discussed possible biologic mechanisms are summarized.

show abstract

Section: Mechanisms Underlying Bpa‐stimulated Carcinogenic Effectsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

2016

View full text Add to dashboard Cite

show abstract

“…Bisphenol A (BPA), one of the endocrine disrupting chemicals (EDCs), is widely used in the manufacture of epoxy resins and polycarbonates, and thus, is a substance ubiquitously found in consumer products, like polycarbonate food containers and utensils, dental sealants, protective coatings, and water supply pipes [7,8]. Reports available now suggest that BPA can interfere with hormone synthesis and hormone receptor expression, specifically alter gene activities in target tissues, which might influence potential genetic embryo stability and immune homeostasis [9][10][11]. According to the latest study, measurable levels of BPA were detected in maternal blood in the USA population, close to a nanomole scale [12].…”

Section: Introductionmentioning

confidence: 99%

MAPK and NF-κB Pathways Are Involved in Bisphenol A-Induced TNF-α and IL-6 Production in BV2 Microglial Cells

et al. 2014

View full text Add to dashboard Cite

Microglial activation has been reported to play an important role in neurodegenerative diseases by producing pro-inflammatory cytokines. Bisphenol A (BPA, 2,2-bis (4-hydroxyphenyl) propane), known as a ubiquitous endocrine-disrupting chemical, is reported to perform both mimic- and anti-estrogen properties; however, whether it affects cytokine production or immune response in central nervous system remains unclear. The present study was aimed to explore whether BPA was involved in inflammatory action and to investigate the potential mechanisms in microglial cells. BV2, the murine microglial cell line, was used in the present work as the cell model. BPA-associated morphologic changes, cytokine responses, and signaling events were examined using immunofluorescence analysis, real-time PCR, enzyme-linked immunosorbent assay, and western blot. Our results indicated that BPA increased BV2 cells activation and simultaneously elevated tumor necrosis factor-α and interleukin 6 expression, which could be partially reversed by estrogen receptor antagonist, ICI182780. In addition, the c-Jun N-terminal protein kinase (JNK) inhibitor (SP600125), rather than ERK1/2 blocker (PD98059), displayed anti-inflammatory properties on BPA-elicited cytokine responses. Moreover, the inflammatory transcription factor NF-κB was specifically activated by BPA as well. These results, taken together, suggested that BPA may have functional effects on the response of microglial cell activation via, in part, the estrogen receptor, JNK, ERK mitogen-activated protein kinase, and NF-κB signaling pathways with its subsequent influence on pro-inflammatory action.

show abstract

“…Exposure to BPA upregulated the expression of Oct4 and Nanog in a dosedependent manner. Furthermore, BPA, but not estradiol, downregulated E-cadherin expression, suggesting that regulation of E-cadherin expression occurred through an estrogen-independent mechanism (Yang et al 2013). Together, these observations suggest that BPA disrupts differentiation by promoting a stem cell phenotype.…”

Section: Mammary Gland Developmentmentioning

confidence: 81%

“…BPA is reported to activate estrogen receptor (ER) signaling in the primary mesenchyme, thereby inducing adipocyte differentiation in periductal stroma and fat pad and promoting ductal elongation and branching (reviewed in detail by Soto et al (2013)). To determine the mechanisms by which BPA exposure modulates mammary gland morphogenesis at the cellular level, the human ES cells X-01 were cultured in the three-dimensional mammosphere assay in the presence of differentiation medium and increasing concentrations of BPA (Yang et al 2013). Exposure to BPA upregulated the expression of Oct4 and Nanog in a dosedependent manner.…”

Section: Mammary Gland Developmentmentioning

confidence: 99%

Actions of endocrine-disrupting chemicals on stem/progenitor cells during development and disease

Kopras

Potluri

Bermúdez

et al. 2013

Endocrine-Related Cancer

View full text Add to dashboard Cite

Development and fate of the stem cell are regulated by extrinsic signals from the environment. Endocrine-disrupting chemicals which perturb hormonal signaling in utero and during early childhood may cause deregulation of multiple developmental processes, ranging from breakdown of stem cell niche architecture, developmental reprograming and altered stem cell fate to impaired organ and gonad development and sexual differentiation. Therefore, study of the environmental effects on stem cell integrity and normal development is a new and emerging focus for developmental biologists and cell toxicologists. When combined with new human and mouse stem cell-based models, stem cell differentiation dynamics can be studied in more biologically relevant ways. In this study, we review the current status of our understanding of the molecular mechanisms by which endocrine disruptors alter embryonic stem cell and adult stem/progenitor cell fate, organ development, cancer stem cell activity, and tumorigenesis.

show abstract

Effect of low dose bisphenol A on the early differentiation of human embryonic stem cells into mammary epithelial cells

Cited by 46 publications

References 57 publications

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

MAPK and NF-κB Pathways Are Involved in Bisphenol A-Induced TNF-α and IL-6 Production in BV2 Microglial Cells

Actions of endocrine-disrupting chemicals on stem/progenitor cells during development and disease

Contact Info

Product

Resources

About