Literature DB >> 24295492

DNA methylation and miRNAs regulation in hereditary breast cancer: epigenetic changes, players in transcriptional and post- transcriptional regulation in hereditary breast cancer.

R Pinto, S De Summa, B Pilato, S Tommasi1.   

Abstract

The genetic alterations associated with breast carcinogenesis are well known. On the contrary epigenetic alterations in hereditary breast cancer are a new field. Two epigenetic mechanisms have emerged as the most critical players in transcriptional regulation in breast cancer: the methylation of DNA and microRNA interference. In this review we will focus on recent findings on gene silencing caused by DNA methylation and microRNA to explore the potential role of these epigenetic changes in the understanding of hereditary breast cancer. Moreover we will describe the same alterations in basal-like breast cancer and in triple-negative breast cancer, since their phenotypes have similarities with BRCA1-mutated tumors. To underline the possibility that some epigenetic alterations could also be used as potential epigenetic biomarkers of drug sensitivity or resistance, we will discuss the more common therapies in hereditary breast cancer that could also be applied to breast cancer with basal-like or triple negative phenotypes.

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Year:  2014        PMID: 24295492     DOI: 10.2174/1566524013666131203101405

Source DB:  PubMed          Journal:  Curr Mol Med        ISSN: 1566-5240            Impact factor:   2.222


  9 in total

1.  LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer.

Authors:  Mingming Lv; Pengfei Xu; Ying Wu; Lei Huang; Wenqu Li; Shanshan Lv; Xiaowei Wu; Xin Zeng; Rong Shen; Xuemei Jia; Yongmei Yin; Yun Gu; Hongyan Yuan; Hui Xie; Ziyi Fu
Journal:  Oncotarget       Date:  2016-03-15

2.  Prognostic value of genome-wide DNA methylation patterns in noncoding miRNAs and lncRNAs in uveal melanomas.

Authors:  Zheng Zheng; Dan Xu; Keqing Shi; Minfeng Chen; Fan Lu
Journal:  Aging (Albany NY)       Date:  2019-08-20       Impact factor: 5.682

3.  DNMT1-mediated methylation inhibits microRNA-214-3p and promotes hair follicle stem cell differentiate into adipogenic lineages.

Authors:  Fangcao Jin; Min Li; Xuyang Li; Yunpeng Zheng; Kun Zhang; Xiaojun Liu; Bingjie Cai; Guangwen Yin
Journal:  Stem Cell Res Ther       Date:  2020-10-19       Impact factor: 6.832

4.  DNA methylation variations in familial female and male breast cancer.

Authors:  Edoardo Abeni; Ilaria Grossi; Eleonora Marchina; Arianna Coniglio; Paolo Incardona; Pietro Cavalli; Fausto Zorzi; Pier Luigi Chiodera; Carlo Terenzio Paties; Marialuisa Crosatti; Giuseppina De Petro; Alessandro Salvi
Journal:  Oncol Lett       Date:  2021-04-12       Impact factor: 2.967

5.  Pregnancy-associated plasma protein-A (PAPPA) promotes breast cancer progression.

Authors:  Jun Zhang; Yuan Zhang; Lanjiang Li; Yinghua Nian; Ying Chen; Ruoxia Shen; Xiaoyan Ma
Journal:  Bioengineered       Date:  2022-01       Impact factor: 3.269

6.  DNA methylation study of fetus genome through a genome-wide analysis.

Authors:  Hong-Dan Wang; Qiao-Fang Hou; Qian-Nan Guo; Tao Li; Dong Wu; Xian-Ping Zhang; Yan Chu; Miao He; Hai Xiao; Liang-Jie Guo; Ke Yang; Shi-Xiu Liao; Bo-Feng Zhu
Journal:  BMC Med Genomics       Date:  2014-04-15       Impact factor: 3.063

Review 7.  Regulatory mechanisms of microRNA expression.

Authors:  Lyudmila F Gulyaeva; Nicolay E Kushlinskiy
Journal:  J Transl Med       Date:  2016-05-20       Impact factor: 5.531

8.  Tamoxifen reverses epithelial-mesenchymal transition by demethylating miR-200c in triple-negative breast cancer cells.

Authors:  Qian Wang; Yu Cheng; Yan Wang; Yibo Fan; Ce Li; Ye Zhang; Yiding Wang; Qian Dong; Yanju Ma; Yue-E Teng; Xiujuan Qu; Yunpeng Liu
Journal:  BMC Cancer       Date:  2017-07-19       Impact factor: 4.430

Review 9.  Role of ctDNA in Breast Cancer.

Authors:  Marta Sant; Adrià Bernat-Peguera; Eudald Felip; Mireia Margelí
Journal:  Cancers (Basel)       Date:  2022-01-09       Impact factor: 6.639

  9 in total

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