Literature DB >> 23194197

Role of melatonin on electromagnetic radiation-induced oxidative stress and Ca2+ signaling molecular pathways in breast cancer.

Mustafa Naziroğlu1, Sümeyye Tokat, Seda Demirci.   

Abstract

AIMS: Exposure to electromagnetic radiation (EMR) may increase breast cancer risk by inducing oxidative stress and suppressing the production of melatonin. Aim of the present review is to discuss the mechanisms and risk factors of EMR and oxidative stress-induced breast cancer, to summarize the controlled studies evaluating measures for prevention, and to conclude with evidence-based strategies for prevention. MATERIALS: Review of the relevant literature and results from our recent basic studies, as well as critical analyses of published systematic reviews were obtained from the Pubmed and the Science Citation Index.
RESULTS: It has been proposed that chronic exposure to EMR may increase the risk of breast cancer by suppressing the production of melatonin; this suppression may affect the development of breast cancer either by increasing levels of circulation of estrogen or through over production of free oxygen radicals. Most epidemiological studies have also indicated overall effect of EMR exposure in premenopausal women, particularly for estrogen receptor positive breast tumors. Enhanced voltage-dependent Ca(2+) current and impaired inhibitory G-protein function, and derangement of intracellular organelles with a Ca(2+) buffering effect, such as endoplasmic reticulum and mitochondria have been also shown to contribute to disturbed Ca(2+) signaling in breast cancer.
CONCLUSION: Melatonin may modulate breast cancer through modulation of enhanced oxidative stress and Ca(2+) influx in cell lines. However, there is not enough evidence on increased risk of breast cancer related to EMR exposure.

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Year:  2012        PMID: 23194197     DOI: 10.3109/10799893.2012.737002

Source DB:  PubMed          Journal:  J Recept Signal Transduct Res        ISSN: 1079-9893            Impact factor:   2.092


  19 in total

1.  Expression of P2X7R in breast cancer tissue and the induction of apoptosis by the gene-specific shRNA in MCF-7 cells.

Authors:  Chao Tan; L I Han; Lili Zou; Chunhua Luo; Aihua Liu; Xiejing Sheng; Dee Xi
Journal:  Exp Ther Med       Date:  2015-08-24       Impact factor: 2.447

Review 2.  Recent reports of Wi-Fi and mobile phone-induced radiation on oxidative stress and reproductive signaling pathways in females and males.

Authors:  Mustafa Nazıroğlu; Murat Yüksel; Seyit Ali Köse; Mehmet Okan Özkaya
Journal:  J Membr Biol       Date:  2013-10-09       Impact factor: 1.843

3.  Reduction in traumatic brain injury-induced oxidative stress, apoptosis, and calcium entry in rat hippocampus by melatonin: Possible involvement of TRPM2 channels.

Authors:  Vehbi Yürüker; Mustafa Nazıroğlu; Nilgün Şenol
Journal:  Metab Brain Dis       Date:  2014-10-23       Impact factor: 3.584

4.  Electromagnetic radiation (Wi-Fi) and epilepsy induce calcium entry and apoptosis through activation of TRPV1 channel in hippocampus and dorsal root ganglion of rats.

Authors:  Vahid Ghazizadeh; Mustafa Nazıroğlu
Journal:  Metab Brain Dis       Date:  2014-05-03       Impact factor: 3.584

5.  Epilepsy but not mobile phone frequency (900 MHz) induces apoptosis and calcium entry in hippocampus of epileptic rat: involvement of TRPV1 channels.

Authors:  Mustafa Nazıroğlu; Fatma Feyza Özkan; Seher Rabia Hapil; Vahid Ghazizadeh; Bilal Çiğ
Journal:  J Membr Biol       Date:  2014-11-09       Impact factor: 1.843

6.  5-Fluorouracil-induced mitochondrial oxidative cytotoxicity and apoptosis are increased in MCF-7 human breast cancer cells by TRPV1 channel activation but not Hypericum perforatum treatment.

Authors:  Haci Ahmet Deveci; Mustafa Nazıroğlu; Gökhan Nur
Journal:  Mol Cell Biochem       Date:  2017-08-09       Impact factor: 3.396

Review 7.  Deregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer: possibilities for therapeutic intervention.

Authors:  Nicole M Davis; Melissa Sokolosky; Kristin Stadelman; Steve L Abrams; Massimo Libra; Saverio Candido; Ferdinando Nicoletti; Jerry Polesel; Roberta Maestro; Antonino D'Assoro; Lyudmyla Drobot; Dariusz Rakus; Agnieszka Gizak; Piotr Laidler; Joanna Dulińska-Litewka; Joerg Basecke; Sanja Mijatovic; Danijela Maksimovic-Ivanic; Giuseppe Montalto; Melchiorre Cervello; Timothy L Fitzgerald; Zoya Demidenko; Alberto M Martelli; Lucio Cocco; Linda S Steelman; James A McCubrey
Journal:  Oncotarget       Date:  2014-07-15

8.  Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis, mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root ganglion of rats.

Authors:  Kemal Ertilav; Fuat Uslusoy; Serdar Ataizi; Mustafa Nazıroğlu
Journal:  Metab Brain Dis       Date:  2018-01-13       Impact factor: 3.584

9.  Extracellular heat shock proteins protect U937 cells from H2O2-induced apoptotic cell death.

Authors:  Lourdes Franco; Jorge Terrinca; Ana B Rodríguez; Javier Espino; José A Pariente
Journal:  Mol Cell Biochem       Date:  2015-11-03       Impact factor: 3.396

Review 10.  TRPV1 Channel: A Potential Drug Target for Treating Epilepsy.

Authors:  Mustafa Nazıroğlu
Journal:  Curr Neuropharmacol       Date:  2015       Impact factor: 7.363

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