Epigenetic mechanisms of breast cancer: an update of the current knowledge

Karslı-Çeppioğlu, Seher; Dagdemir, Aslihan; Judes, Gaëlle; Ngollo, Marjolaine; Penault‐Llorca, Frédérique; Pajon, Amaury; Bignon, Yves‐Jean; Bernard‐Gallon, Dominique

doi:10.2217/epi.14.59

Cited by 97 publications

(71 citation statements)

References 92 publications

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“…Methylation-mediated silencing of tumor suppressor genes can contribute to the establishment and maintenance of the malignant phenotype (12, 13). High levels of DNA methylation occur in invasive and in situ carcinomas (14-19), asymptomatic breasts of high risk compared to average risk women (15-17, 20), and in normal breast tissue 2-4 cm distant to tumor (16, 21, 22).…”

Section: Introductionmentioning

confidence: 99%

Gene Methylation and Cytological Atypia in Random Fine-Needle Aspirates for Assessment of Breast Cancer Risk

Stearns

Fackler

Hafeez

et al. 2016

Cancer Prevention Research

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Methods to determine individualized breast cancer risk lack sufficient sensitivity to select women most likely to benefit from preventive strategies. Alterations in DNA methylation occur early in breast cancer. We hypothesized that cancer-specific methylation markers could enhance breast cancer risk assessment. We evaluated 380 women without a history of breast cancer. We determined their menopausal status or menstrual cycle phase, risk of developing breast cancer (Gail model), and breast density, and obtained random fine needle aspiration (rFNA) samples for assessment of cytopathology and cumulative methylation index (CMI). Eight methylated gene markers were identified through whole genome methylation analysis and included novel and previously established breast cancer detection genes. We performed correlative and multivariate linear regression analyses to evaluate DNA methylation of a gene panel as a function of clinical factors associated with breast cancer risk. CMI and individual gene methylation were independent of age, menopausal status or menstrual phase, lifetime Gail risk score, and breast density. CMI and individual gene methylation for the eight genes increased significantly (p<0.001) with increasing cytological atypia. The findings were verified with multivariate analyses correcting for age, log (Gail), log (percent density), rFNA cell number and BMI. Our results demonstrate a significant association between cytological atypia and high CMI, which does not vary with menstrual phase or menopause and is independent of Gail risk and mammographic density. Thus CMI is an excellent candidate breast cancer risk biomarker, warranting larger prospective studies to establish its utility for cancer risk assessment.

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Section: Introductionmentioning

confidence: 99%

Gene Methylation and Cytological Atypia in Random Fine-Needle Aspirates for Assessment of Breast Cancer Risk

Stearns

Fackler

Hafeez

et al. 2016

Cancer Prevention Research

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“…Anomalous apoptotic responses are prominent in the development and progression of many types of human cancers (17,18). One of the chemopreventive strategies in the treatment of cancer is the induction of apoptotic cell death (7).…”

Section: Discussionmentioning

confidence: 99%

Cnidium officinale Makino extract induces apoptosis through activation of caspase-3 and p53 in human liver cancer HepG2 cells

Hong

Cruz

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. A number of diverse studies have reported the anticancer properties of Cnidium officinale Makino (CO). However, the apoptotic effect of this traditional medicinal herb in human hepatocellular carcinoma cells (HepG2) remains to be elucidated. Therefore, the present study investigated the ability of CO to reduce cell viability through apoptotic pathways. Cell viability was determined using the 2,3-bis [2-methyloxy-4-nitro-5-sulfophenyl]-2H-tetrazolium-5-carboxanilide assay. CO extract-induced apoptosis in HepG2 cells was assessed by Hoechst 33258 staining. The cell cycle was monitored using fluorescence-activated cell sorting analysis with propidium iodide staining. Furthermore, the present study explored whether various signaling molecules associated with HepG2 cell death were affected by CO treatment, including caspase-3, B-cell lymphoma 2 (Bcl-2), tumor protein p53 (p53), cyclin-dependent kinase 4 (CDK4) and cyclin D. The expression levels of these genes were examined by reverse-transcription polymerase chain reaction and western blotting. The expression levels of caspase-3 and p53 were upregulated with CO extract treatment, whereas those of Bcl-2, CDK4 and cyclin D were significantly downregulated. Cleaved caspase-3 expression was upregulated following treatment with CO extract in a dose-dependent manner. Collectively, the data suggest that CO extract has the potential to induce apoptosis of HepG2 cells and may act by suppressing the cell cycle, which leads to caspase-3 cleavage and p53 signaling.

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“…The glucolytic pathway for ATP generation is unable to produce sufficient energy for the normal renewal of the base pairs of eukaryotic cell genes. At this time, normal base pairs are replaced by abnormal base pairs, resulting in gene mutations, DNA methylation, overexpression and no or reduced expression (9)(10)(11)(12). Different chromosomes exhibit different abilities to tolerate the shortage of energy, with some chromosomes being more vulnerable compared with others.…”

Section: The Process Leading To Genes Expressing Characteristics Of Ementioning

confidence: 99%

Association between shortage of energy supply and nuclear gene mutations leading to carcinomatous transformation

2015

Molecular and Clinical Oncology

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Abstract. Anaerobic bacteria use glycolysis, an oxygen-independent metabolic pathway, whereas energy metabolism in the evolved eukaryotic cell is performed via oxidative phosphorylation, with all eukaryotic cell activities depending upon high energy consumption. However, in cancer cells evolving from eukaryotic cells, the energy metabolism switches from oxidative phosphorylation to glycolysis. The shortage of energy supply induces cancer cells to acquire specific characteristics. Base pair renewal is the most energy-consuming process in the cell, and shortage of energy supply may lead to errors in this process; the more prominent the shortage in energy supply, the more errors are likely to occur in base pair renewal, resulting in gene mutations and expression of cancer cell characteristics. Thus, shortage of energy supply is associated with carcinomatous transformation.

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Epigenetic mechanisms of breast cancer: an update of the current knowledge

Cited by 97 publications

References 92 publications

Gene Methylation and Cytological Atypia in Random Fine-Needle Aspirates for Assessment of Breast Cancer Risk

Gene Methylation and Cytological Atypia in Random Fine-Needle Aspirates for Assessment of Breast Cancer Risk

Cnidium officinale Makino extract induces apoptosis through activation of caspase-3 and p53 in human liver cancer HepG2 cells

Association between shortage of energy supply and nuclear gene mutations leading to carcinomatous transformation

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