Bisphenol A-Induced Cell Proliferation and Mitochondrial Oxidative Stress Are Diminished via Modulation of TRPV1 Channel in Estrogen Positive Breast Cancer Cell by Selenium Treatment

Güzel, Kadriye Görkem Ulu; Nazıroğlu, Mustafa; Ceyhan, Derya

doi:10.1007/s12011-020-02057-3

Cited by 10 publications

(4 citation statements)

References 43 publications

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“…BPA has hormone-like properties and can mimic estrogen and interact with its receptors; it can thereby modulate cell proliferation, apoptosis, and migration and contribute to carcinogenesis [131]. However, the proliferative and oxidative effects of BPA, enhanced through TRPV1 activation, are reduced by sodium selenite (Na-Se), which attenuates BPA-induced increases in cell number, mitochondrial oxidative stress, and modulation of TRPV1 channel activity in MCF-7 cells [132]. Interestingly, despite the function of both capsaicin and 6-gingerol as TRPV1 agonists, the two compounds exhibit opposing effects on cancerous cells.…”

Section: Trpv1 As a Potential Target For Anti-cancer Therapiesmentioning

confidence: 99%

Calcium Entry through TRPV1: A Potential Target for the Regulation of Proliferation and Apoptosis in Cancerous and Healthy Cells

Zhai

Líšková

Kubatka

et al. 2020

IJMS

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Intracellular calcium (Ca2+) concentration ([Ca2+]i) is a key determinant of cell fate and is implicated in carcinogenesis. Membrane ion channels are structures through which ions enter or exit the cell, depending on the driving forces. The opening of transient receptor potential vanilloid 1 (TRPV1) ligand-gated ion channels facilitates transmembrane Ca2+ and Na+ entry, which modifies the delicate balance between apoptotic and proliferative signaling pathways. Proliferation is upregulated through two mechanisms: (1) ATP binding to the G-protein-coupled receptor P2Y2, commencing a kinase signaling cascade that activates the serine-threonine kinase Akt, and (2) the transactivation of the epidermal growth factor receptor (EGFR), leading to a series of protein signals that activate the extracellular signal-regulated kinases (ERK) 1/2. The TRPV1-apoptosis pathway involves Ca2+ influx and efflux between the cytosol, mitochondria, and endoplasmic reticulum (ER), the release of apoptosis-inducing factor (AIF) and cytochrome c from the mitochondria, caspase activation, and DNA fragmentation and condensation. While proliferative mechanisms are typically upregulated in cancerous tissues, shifting the balance to favor apoptosis could support anti-cancer therapies. TRPV1, through [Ca2+]i signaling, influences cancer cell fate; therefore, the modulation of the TRPV1-enforced proliferation–apoptosis balance is a promising avenue in developing anti-cancer therapies and overcoming cancer drug resistance. As such, this review characterizes and evaluates the role of TRPV1 in cell death and survival, in the interest of identifying mechanistic targets for drug discovery.

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Section: Trpv1 As a Potential Target For Anti-cancer Therapiesmentioning

confidence: 99%

Calcium Entry through TRPV1: A Potential Target for the Regulation of Proliferation and Apoptosis in Cancerous and Healthy Cells

Zhai

Líšková

Kubatka

et al. 2020

IJMS

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“…Guzel et al, conducted that there was an increase in intracellular Ca 2+ ion, apoptosis, and mitochondrial oxidative stress in MCF-7 cells after exposure to BPH-A. In another study, it was stated that the use of Na-Se reduced cellular damage caused by BPH-A exposure (Guzel et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

“…Studies on BPH-A have shown that it has many harms, including possible carcinogenic effects (Cimmino et al, 2020;Rochester, 2013). The most important damage mechanism of BPH-A in cellular structures is oxidative stress as a consequence of increased intracellular ROS level (Guzel et al, 2020). ROS, a metabolic product, is formed in the process of cells' survival.…”

Section: Discussionmentioning

confidence: 99%

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Protective role of selenium against bisphenol-A induced oxidative stress, cytokine generation and apoptosis in SH-SY5Y neuronal cell line

Yıldızhan

2020

Journal of Cellular Neuroscience and Oxidative Stress

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Journal of Cellular Neuroscience and Oxidative Stress is an online journal that publishes original research articles, reviews and short reviews on the molecular basis of biophysical, physiological and pharmacological processes that regulate cellular function, and the control or alteration of these processes by the action of receptors, neurotransmitters, second messengers, cation, anions, drugs or disease.Areas of particular interest are four topics. They are;A-Ion Channels (Na + -K + Channels, Clchannels, Ca 2+ channels, ADP-Ribose and metabolism of NAD + , Patch-Clamp applications) B-Oxidative Stress (Antioxidant vitamins, antioxidant enzymes, metabolism of nitric oxide, oxidative stress, biophysics, biochemistry and physiology of free oxygen radicals) C-Interaction Between Oxidative Stress and Ion Channels in Neuroscience (Effects of the oxidative stress on the activation of the voltage sensitive cation channels, effect of ADP-Ribose and NAD + on activation of the cation channels which are sensitive to voltage, effect of the oxidative stress on activation of the TRP channels in neurodegenerative diseases such Parkinson's and Alzheimer's diseases) D-Gene and Oxidative Stress (Gene abnormalities. Interaction between gene and free radicals. Gene anomalies and iron. Role of radiation and cancer on gene polymorphism)

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Metabolism and Anticancer Mechanisms of Selocompounds: Comprehensive Review

Dávila-Vega

Gastelum-Hernández

Serrano‐Sandoval

et al. 2022

Biol Trace Elem Res

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Bisphenol A-Induced Cell Proliferation and Mitochondrial Oxidative Stress Are Diminished via Modulation of TRPV1 Channel in Estrogen Positive Breast Cancer Cell by Selenium Treatment

Cited by 10 publications

References 43 publications

Calcium Entry through TRPV1: A Potential Target for the Regulation of Proliferation and Apoptosis in Cancerous and Healthy Cells

Calcium Entry through TRPV1: A Potential Target for the Regulation of Proliferation and Apoptosis in Cancerous and Healthy Cells

Protective role of selenium against bisphenol-A induced oxidative stress, cytokine generation and apoptosis in SH-SY5Y neuronal cell line

Metabolism and Anticancer Mechanisms of Selocompounds: Comprehensive Review

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