Effects of high-dose bisphenol A on the mouse oral mucosa: A possible link with oral cancers

Almeida, Tatiana Fernandes Araújo; Oliveira, Sicília Rezende; Silva, Janine Mayra da; Oliveira, Ana Laura Fernandes de; Cardeal, Zenilda de Lourdes; Menezes, Helvécio Costa; Gomes, José Messias; Campolina-Silva, Gabriel Henrique; Oliveira, Cleida A.; Macari, Soraia; Garlet, Gustavo; Diniz, Ivana Márcia Alves; Leopoldino, Andréia Machado; Silva, Tarcı́lia Aparecida

doi:10.1016/j.envpol.2021.117296

Cited by 12 publications

(7 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…31,[280][281][282] In addition, BPA has been shown to upregulate anti-apoptotic proteins and downregulate pro-apoptotic proteins in several human cancer cell lines. 31 Exposure to BPA was found to significantly increase the growth of human umbilical vascular endothelial cells and the number of segments and nodes of vessel-like structures in one study, 283 and to upregulate genes important for vascularization and angiogenesis in another study. 284 BPA exposure also increased expression of vascular endothelial growth factor in estrogen-sensitive breast cancer cells.…”

Section: Kc3mentioning

confidence: 95%

Application of the Key Characteristics of Carcinogens to Bisphenol A

Ricker,

Cheng,

Hsieh

et al. 2024

Int J Toxicol

View full text Add to dashboard Cite

The ten key characteristics (KCs) of carcinogens are based on characteristics of known human carcinogens and encompass many types of endpoints. We propose that an objective review of the large amount of cancer mechanistic evidence for the chemical bisphenol A (BPA) can be achieved through use of these KCs. A search on metabolic and mechanistic data relevant to the carcinogenicity of BPA was conducted and web-based software tools were used to screen and organize the results. We applied the KCs to systematically identify, organize, and summarize mechanistic information for BPA, and to bring relevant carcinogenic mechanisms into focus. For some KCs with very large data sets, we utilized reviews focused on specific endpoints. Over 3000 studies for BPA from various data streams (exposed humans, animals, in vitro and cell-free systems) were identified. Mechanistic data relevant to each of the ten KCs were identified, with receptor-mediated effects, epigenetic alterations, oxidative stress, and cell proliferation being especially data rich. Reactive and bioactive metabolites are also associated with a number of KCs. This review demonstrates how the KCs can be applied to evaluate mechanistic data, especially for data-rich chemicals. While individual entities may have different approaches for the incorporation of mechanistic data in cancer hazard identification, the KCs provide a practical framework for conducting an objective examination of the available mechanistic data without a priori assumptions on mode of action. This analysis of the mechanistic data available for BPA suggests multiple and inter-connected mechanisms through which this chemical can act.

show abstract

Section: Kc3mentioning

confidence: 95%

Application of the Key Characteristics of Carcinogens to Bisphenol A

Ricker,

Cheng,

Hsieh

et al. 2024

Int J Toxicol

View full text Add to dashboard Cite

show abstract

“…BPA agonistic action on ER triggers cell proliferation, invasion, and migration through G-protein related intracellular signaling [ 83 ]. Prolonged exposure of BPA was also proven to modify mucosal architecture inducing preneoplastic changes in murine oral cavity [ 84 ]. BPA pro-oncogenic role was clarified through in vitro demonstration of BPA-induced expression of metalloproteinases and growth factors, enhancing cell proliferation and angiogenesis, while decreasing apoptosis [ 85 , 86 , 87 , 88 ].…”

Section: Bisphenol a Effects On Human Healthmentioning

confidence: 99%

Current Evidence on Bisphenol A Exposure and the Molecular Mechanism Involved in Related Pathological Conditions

et al. 2023

View full text Add to dashboard Cite

Bisphenol A (BPA) is one of the so-called endocrine disrupting chemicals (EDCs) and is thought to be involved in the pathogenesis of different morbid conditions: immune-mediated disorders, type-2 diabetes mellitus, cardiovascular diseases, and cancer. The purpose of this review is to analyze the mechanism of action of bisphenol A, with a special focus on mesenchymal stromal/stem cells (MSCs) and adipogenesis. Its uses will be assessed in various fields: dental, orthopedic, and industrial. The different pathological or physiological conditions altered by BPA and the related molecular pathways will be taken into consideration.

show abstract

“…To a much lesser extent, studies on two other types of epigenetic changes, including histone modifications and noncoding RNAs dysregulation, have also been conducted, although primarily in cell culture systems and animal models [106,120,218,219]. The histone modification studies have focused on representative active or repressive histone marks (e.g., H3K4me, H3K9ac or H3K9me3, and H3K27me3), also measuring enzymes that catalyze these reactions, including histone acetyltransferases (HATs), histone methyltransferases (HMTs), histone deacetylases (HDACs), and histone demethylases (KDMs), and quantifying the expression of associated genes [139,164,167,186,196,[220][221][222][223][224][225][226][227][228][229][230][231][232][233][234][235][236]. For instance, BPA treatment of human breast cancer cells (MCF7) resulted in increased histone acetylation and H3K4 trimethylation through enrichment of the mixed-lineage leukemia family of histone methyltransferases (MLL2 and MLL3) and CREB-binding protein and p300 (CBP/p300; paralogous lysine acetyltransferases) at the promoter of HOXC6, HOXB9, and the enhancer of Zeste homolog 2 (EZH2) that are involved in breast cancer and other types of cancer [222,223,227].…”

Section: Epigenetic Effects Of Bpamentioning

confidence: 99%

“…For instance, BPA treatment of human breast cancer cells (MCF7) resulted in increased histone acetylation and H3K4 trimethylation through enrichment of the mixed-lineage leukemia family of histone methyltransferases (MLL2 and MLL3) and CREB-binding protein and p300 (CBP/p300; paralogous lysine acetyltransferases) at the promoter of HOXC6, HOXB9, and the enhancer of Zeste homolog 2 (EZH2) that are involved in breast cancer and other types of cancer [222,223,227]. Furthermore, primary human endometrial cells and several other cancer cell lines treated with BPA showed significant changes in global histone acetylation and methylation (H3K9ac, H3K9me3, H3K4me3, H3K18/23 diacetylation, H3K27me3, or H4K20me3) [139,164,232,233,235]. In addition, BPA treatment significantly changed the expression levels of various HDACs, including HDAC1, HDAC3, HDAC5, and HDAC7, and HATs in both normal and cancer cell lines [139,232,233,235].…”

Section: Epigenetic Effects Of Bpamentioning

confidence: 99%

The State of Research and Weight of Evidence on the Epigenetic Effects of Bisphenol A

Besaratinia

2023

IJMS

View full text Add to dashboard Cite

Bisphenol A (BPA) is a high-production-volume chemical with numerous industrial and consumer applications. BPA is extensively used in the manufacture of polycarbonate plastics and epoxy resins. The widespread utilities of BPA include its use as internal coating for food and beverage cans, bottles, and food-packaging materials, and as a building block for countless goods of common use. BPA can be released into the environment and enter the human body at any stage during its production, or in the process of manufacture, use, or disposal of materials made from this chemical. While the general population is predominantly exposed to BPA through contaminated food and drinking water, non-dietary exposures through the respiratory system, integumentary system, and vertical transmission, as well as other routes of exposure, also exist. BPA is often classified as an endocrine-disrupting chemical as it can act as a xenoestrogen. Exposure to BPA has been associated with developmental, reproductive, cardiovascular, neurological, metabolic, or immune effects, as well as oncogenic effects. BPA can disrupt the synthesis or clearance of hormones by binding and interfering with biological receptors. BPA can also interact with key transcription factors to modulate regulation of gene expression. Over the past 17 years, an epigenetic mechanism of action for BPA has emerged. This article summarizes the current state of research on the epigenetic effects of BPA by analyzing the findings from various studies in model systems and human populations. It evaluates the weight of evidence on the ability of BPA to alter the epigenome, while also discussing the direction of future research.

show abstract

Effects of high-dose bisphenol A on the mouse oral mucosa: A possible link with oral cancers

Cited by 12 publications

References 69 publications

Application of the Key Characteristics of Carcinogens to Bisphenol A

Application of the Key Characteristics of Carcinogens to Bisphenol A

Current Evidence on Bisphenol A Exposure and the Molecular Mechanism Involved in Related Pathological Conditions

The State of Research and Weight of Evidence on the Epigenetic Effects of Bisphenol A

Contact Info

Product

Resources

About