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

Lei, Bingli; Tang, Qianqian; Sun, Shuming; Zhang, Xiaolan; Huang, Yaoyao; Xu, Lanbing

doi:10.1016/j.envpol.2021.116636

Cited by 14 publications

(13 citation statements)

References 47 publications

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“…These findings indicated that TCBPA and BPAF at the test concentrations activated PI3K/Akt and its downstream signal targets via GPER1-EGFR at the mRNA level, which further regulated the migration of SK-BR-3 cells induced by TCBPA and BPAF. Furthermore, our previous studies found that BPAF at 0.01 μM and TCBPA at 1 μM upregulated the expression of GPER1 protein and increased the phosphorylation of Akt and ERK1/2, 31,32 which further confirmed the role of the activation of PI3K/Akt signaling pathways via GPER1 in regulating BPAF-and TCBPA-induced SK-BR-3 cell migration.…”

Section: Discussionsupporting

confidence: 60%

“…Our previous study revealed that TCBPA and BPAF upregulated the protein expression associated with GPER1-mediated PI3K/Akt and its downstream signals. 31,32 In this study, GPER1-mediated PI3K/Akt and its downstream signals were also selected as the main target genes in mRNA expression detection. We found that TCBPA at 0.1 and 1 μM upregulated mRNA expression of most of the 18 targets, such as GPER1, EGFR, Akt, MAPKs, and their downstream targets (Figure 2).…”

Section: Tcbpa and Bpaf Elevated Mrna Levels Of Targets In Sk-br-3 Cellsmentioning

confidence: 99%

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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

Lei

et al. 2022

Environmental Toxicology

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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. We found that low‐concentration BPAF and TCBPA markedly accelerated the migration of SK‐BR‐3 cells and elevated the mRNA levels of target genes associated with PI3K/Akt and mitogen‐activated protein kinase (MAPK) signals. TCBPA‐ and BPAF‐induced upregulation of target genes was significantly reduced by GPER1 inhibitor G15, the PI3K/Akt inhibitor wortmannin (WM), and the epidermal growth factor receptor (EGFR) inhibitor ZD1839 (ZD). G15 and WM also decreased cell migration induced by TCBPA and BPAF. The findings revealed that TCBPA and BPAF promoted SK‐BR‐3 cell migration ability by activating PI3K/Akt signaling pathway via GPER1‐EGFR.

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Section: Discussionsupporting

confidence: 60%

Section: Tcbpa and Bpaf Elevated Mrna Levels Of Targets In Sk-br-3 Cellsmentioning

confidence: 99%

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

Lei

et al. 2022

Environmental Toxicology

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“…TGFB1, MYC, ErbB, BRCA1, EGFR ). Various studies confirm changes in the expression of these genes or proteins upon bisphenol exposure: in breast cancer cell lines, low concentrations of BPAF [ 61 ] and tetrachloro-BPA [ 62 ] enhanced protein expression of c-Myc and cyclin D1, important for cell cycle progression. In mice, this led to an activation of epidermal growth factor receptor (EGFR) and subsequent increases in growth factor expression related to mammary carcinoma [ 63 ].…”

Section: Discussionmentioning

confidence: 99%

Different bisphenols induce non-monotonous changes in miRNA expression and LINE-1 methylation in two cell lines

Oldenburg

Fürhacker

Hartmann

et al. 2021

Environmental Epigenetics

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4,4ʹ-Isopropylidenediphenol (bisphenol A, BPA), a chemical substance that is widely used mainly as a monomer in the production of polycarbonates, in epoxy resins, and in thermal papers, is suspected to cause epigenetic modifications with potentially toxic consequences. Due to its negative health effects, BPA is banned in several products and is replaced by other bisphenols such as bisphenol S and bisphenol F. The present study examined the effects of BPA, bisphenol S, bisphenol F, p,pʹ-oxybisphenol, and the BPA metabolite BPA β-d-glucuronide on the expression of a set of microRNAs (miRNAs) as well as long interspersed nuclear element-1 methylation in human lung fibroblast and Caco-2 cells. The results demonstrated a significant modulation of the expression of different miRNAs in both cell lines including miR-24, miR-155, miR-21, and miR-146a, known for their regulatory functions of cell cycle, metabolism, and inflammation. At concentrations between 0.001 and 10 µg/ml, especially the data of miR-155 and miR-24 displayed non-monotonous and often significant dose–response curves that were U- or bell-shaped for different substances. Additionally, BPA β-d-glucuronide also exerted significant changes in the miRNA expression. miRNA prediction analysis indicated effects on multiple molecular pathways with relevance for toxicity. Besides, long interspersed nuclear element-1 methylation, a marker for the global DNA methylation status, was significantly modulated by two concentrations of BPA and p,pʹ-oxybisphenol. This pilot study suggests that various bisphenols, including BPA β-d-glucuronide, affect epigenetic mechanisms, especially miRNAs. These results should stimulate extended toxicological studies of multiple bisphenols and a potential use of miRNAs as markers.

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“…4A). CCK-8 results of 1 μM and 10 μM groups were much closer to DMSO group, so taking the official manual of ICI 182,780 and former published research [11] into consideration, we used 1 μM for subsequent experiments. The upregulation of c-myc was blocked by the oestrogen receptor inhibitor (P < 0.05), but had no significant effect on the protein (Fig.…”

Section: Effects Of Rhein On Estrogen Signaling Pathway and C-myc Levelmentioning

confidence: 99%

Rhein promotes the proliferation of keratinocytes by targeting oestrogen receptors for skin ulcer treatment

Chen

Guo

et al. 2022

BMC Complement Med Ther

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Background The Sheng-ji Hua-yu (SJHY) formula is a quite effective Traditional Chinese Medicines (TCM) in the treatment of delayed diabetic wounds. Previous research has shown that the SJHY formula has significant anti-inflammatory and wound-healing effects, but the precise mechanism remains unknown. The purpose of this study was to evaluate the effects of rhein, a compound extracted from SJHY formula, in keratinocytes and to investigate the underlying mechanisms. Methods Microscale thermophoresis (MST) technology was used to confirm that rhein binds directly to oestrogen receptors (ERs). Rhein was then used to treat keratinocytes in vitro. Cell cycle and proliferation analysis, Real-time polymerase chain reaction (RT-PCR) and Western-blot were conducted. Results Rhein increased the proportion of cells in the S phase of the cell cycle and promoted keratinocyte proliferation. ICI 182,780, an ER inhibitor, was also used to treat keratinocytes. The expression of c-myc mRNA and protein induced by rhein was antagonized by ICI 182,780, indicating that this induction is ER dependent. Intervention with ICI 182,780 had no effect on the upregulation of FosB and JunD, indicating that activator protein 1 (AP-1) members (FosB and JunD) are involved in rhein-induced c-myc mRNA and protein expression but does not require the ER. Conclusion The present study found that rhein stimulates keratinocyte proliferation by activating the oestrogen signalling pathway via the oestrogen receptor, which induces the expression of c-myc in collaboration with FosB and JunD, thereby accelerating the process of re-epithelialization.

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

Cited by 14 publications

References 47 publications

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

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 bisphenols induce non-monotonous changes in miRNA expression and LINE-1 methylation in two cell lines

Rhein promotes the proliferation of keratinocytes by targeting oestrogen receptors for skin ulcer treatment

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