Effects of trichlorobisphenol A on the expression of proteins and genes associated with puberty initiation in GT1-7 cells and the relevant molecular mechanism.

This study evaluated the effects of ClBPA on kisspeptin-G-protein coupled receptor 54 (GPR54)/gonadotropin-releasing hormone (GnRH) (KGG) signals and analyzed the roles of estrogen receptor alpha (ERɑ) and G-protein coupled estrogen receptor 1 (GPER1) in regulating KGG signals. The results showed that ClBPA at 50 μM increased the levels of intracellular reactive oxygen species (ROS) and GnRH, upregulated the protein levels of kisspeptin and the expression of fshr, lhr and gnrh1 genes related to KGG in GT1-7 cells. In addition, 50 μM ClBPA significantly upregulated the phosphorylation of extracellular regulated protein kinases 1/2 (Erk1/2), the protein levels of GPER1 and the expression of the gper1 as well as the most target genes associated with mitogen-activated protein kinase (MAPK)/Erk1/2 pathways.

Molecular insights into the effects of tetrachlorobisphenol A on puberty initiation in Wistar rats.

Tetrachlorobisphenol A (TCBPA) is the chlorinated derivative of bisphenol A (BPA). Several studies have found that BPA adversely affects the reproductive activity largely through binding to estrogen receptors and the critical period of BPA exposure advances the vaginal opening time in the female offspring via the kisspeptin/G protein-coupled receptor 54 (KGG) system. However, whether TCBPA can affect puberty initiation via KGG and the roles of estrogen receptors in this process remain unknown.

Bisphenol AF Promoted the Growth of Uterus and Activated Estrogen Signaling Related Targets in Various Tissues of Nude Mice with SK-BR-3 Xenograft Tumor.

Environmental estrogens can promote the growth, migration, and invasion of breast cancer. However, few studies evaluate adverse health impacts of environmental estrogens on other organs of breast cancer patients. Therefore, the present study investigated the effects of environmental estrogen bisphenol AF (BPAF) on the main organs of female Balb/cA nude mice with SK-BR-3 xenograft tumor by detecting the organ development and gene expression of targets associated with G protein-coupled estrogen receptor 1 (GPER1)-mediated phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) and mitogen-activated protein kinase (MAPK) signaling pathways in hypothalamus, ovary, uterus, liver, and kidney.

Tetrachlorobisphenol A and bisphenol AF induced cell migration by activating PI3K/Akt signaling pathway via G protein-coupled estrogen receptor 1 in SK-BR-3 cells.

Different subtypes of breast cancer express positively G protein-coupled estrogen receptor 1 (GPER1). Our previous studies found that tetrachlorobisphenol A (TCBPA) and bisphenol AF (BPAF) significantly promoted SK-BR-3 cell proliferation by activating GPER1-regulated signals. The present study further investigated the effects of TCBPA and BPAF on the migration of SK-BR-3 cells and examined the role of phosphatidylinositol 3-kinase-protein kinase B (PI3K/Akt) and its downstream signal targets in this process.

Chlorobisphenol A activated kisspeptin/GPR54-GnRH neuroendocrine signals through ERα and GPER pathway in neuronal GT1-7 cells.

Chlorobisphenol A (ClBPA) is a kind of novel estrogenic compounds. The present study aims to investigate the effects of three ClBPA compounds on the kisspeptin/G protein-coupled receptor 54 (GPR54, also named KissR1)-gonadotropin-releasing hormone (GnRH) (KGG) system in neuronal GT1-7 cells with mechanistic insights by estrogen receptor signaling pathways. The study demonstrated that low-concentration ClBPA induced the cell proliferation, promoted GnRH secretion, upregulated the expression of KGG neuroendocrine signal-related proteins (KissR1, GnRH1 and kisspeptin) and genes including Kiss1, GnRH1, KissR1, luteinizing hormone receptor (Lhr) and follicle-stimulating hormone receptor (Fshr) in GT1-7 cells.

Molecular mechanism study of BPAF-induced proliferation of ERα-negative SKBR-3 human breast cancer cells in vitro/in vivo.

Bisphenol AF (BPAF) is a known estrogen disruptor of the ERα pathway. The aim of the present study was to characterize the proliferation effects of BPAF on ERα-negative SKBR-3 breast cancer cells with mechanistic insights. BPAF at low concentrations (0.

Insight into the mechanism of tetrachlorobisphenol A (TCBPA)-induced proliferation of breast cancer cells by GPER-mediated signaling pathways.

Tetrachlorobisphenol A (TCBPA), a chlorinated derivative of bisphenol A, is an endocrine disruptor based on interaction with nuclear estrogen receptor alpha (ERα). However, there is only limited data on the mechanisms through which TCBPA-associated estrogenic activity is related to the membrane G protein-coupled estrogen receptor (GPER) pathway. In this study, three human breast cancer cell lines-MCF-7, SKBR3, and MDA-MB-231 cells were used to evaluate whether, as well as how, TCBPA at concentration range of 0.

The proliferation effects of fluoxetine and amitriptyline on human breast cancer cells and the underlying molecular mechanisms.

Some studies have suggested possible estrogen actions for antidepressants such as fluoxetine. However, the specific molecular mechanisms remain unclear. In this study, the molecular mechanism of fluoxetine-induced the proliferation of breast cancer SKBR3 and MCF-7 cells was evaluated by detecting ERα and GPR30-mediated ERK and PI3K/AKT signals.

A Method for Detecting Dynamic Mutation of Complex Systems Using Improved Information Entropy.

In this study, a nonlinear analysis method called improved information entropy (IIE) is proposed on the basis of constructing a special probability mass function for the normalized analysis of Shannon entropy for a time series. The definition is directly applied to several typical time series, and the characteristic of IIE is analyzed. This method can distinguish different kinds of signals and reflects the complexity of one-dimensional time series of high sensitivity to the changes in signal.