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      Transcriptome sequencing of adenomyosis eutopic endometrium: A new insight into its pathophysiology

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          The eutopic endometrium has been suggested to play a crucial role in the pathogenesis of adenomyosis. However, the specific genes in eutopic endometrium responsible for the pathogenesis of adenomyosis still remain to be elucidated. We aim to identify differentially expressed genes (DEGs) and molecular pathways/networks in eutopic endometrium from adenomyosis patients and provide a new insight into disease mechanisms at transcriptome level. RNA sequencing (RNA‐Seq) was performed with 12 eutopic endometrium from adenomyosis and control groups. Differentially expressed genes in adenomyosis were validated by quantitative real‐time PCR (qPCR) and immunochemistry. Functional annotations of the DEGs were analysed with Ingenuity Pathway Analysis (IPA). Quantitative DNA methylation analysis of CEBPB was performed with MassArray system. A total of 373 differentially expressed genes were identified in the adenomyosis eutopic endometrium compared to matched controls. Bioinformatic analysis predicted that IL‐6 signalling and ERK/MAPK signalling were activated in adenomyosis endometrium. We also found that the increased expression and DNA hypomethylation of CEBPB were associated with adenomyosis. Our results revealed key pathways and networks in eutopic endometrium of adenomyosis. The study is the first to propose the association between C/EBPβ and adenomyosis and can improve the understanding of the pathogenesis of adenomyosis.

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          Most cited references 23

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          Role of DNA Methylation in Modulating Transcription Factor Occupancy.

          Although DNA methylation is commonly invoked as a mechanism for transcriptional repression, the extent to which it actively silences transcription factor (TF) occupancy sites in vivo is unknown. To study the role of DNA methylation in the active modulation of TF binding, we quantified the effect of DNA methylation depletion on the genomic occupancy patterns of CTCF, an abundant TF with known methylation sensitivity that is capable of autonomous binding to its target sites in chromatin. Here, we show that the vast majority (>98.5%) of the tens of thousands of unoccupied, methylated CTCF recognition sequences remain unbound upon abrogation of DNA methylation. The small fraction of sites that show methylation-dependent binding in vivo are in turn characterized by highly variable CTCF occupancy across cell types. Our results suggest that DNA methylation is not a primary groundskeeper of genomic TF landscapes, but rather a specialized mechanism for stabilizing intrinsically labile sites.
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            CCAAT/enhancer-binding protein beta: its role in breast cancer and associations with receptor tyrosine kinases.

            The CCAAT/enhancer-binding proteins (C/EBPs) are a family of leucine-zipper transcription factors that regulate gene expression to control cellular proliferation, differentiation, inflammation and metabolism. Encoded by an intronless gene, C/EBPbeta is expressed as several distinct protein isoforms (LAP1, LAP2, LIP) whose expression is regulated by the differential use of several in-frame translation start sites. LAP1 and LAP2 are transcriptional activators and are associated with differentiation, whereas LIP is frequently elevated in proliferative tissue and acts as a dominant-negative inhibitor of transcription. However, emerging evidence suggests that LIP can serve as a transcriptional activator in some cellular contexts, and that LAP1 and LAP2 might also have unique actions. The LIP:LAP ratio is crucial for the maintenance of normal growth and development, and increases in this ratio lead to aggressive forms of breast cancer. This review discusses the regulation of C/EBPbeta activity by post-translational modification, the individual actions of LAP1, LAP2 and LIP, and the functions and downstream targets that are unique to each isoform. The role of the C/EBPbeta isoforms in breast cancer is discussed and emphasis is placed on their interactions with receptor tyrosine kinases.
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              DNA methylation in development and human disease.

              DNA methylation is a heritable and stable epigenetic mark associated with transcriptional repression. Changes in the patterns and levels of global and regional DNA methylation regulate development and contribute directly to disease states such as cancer. Recent findings provide intriguing insights into the epigenetic crosstalk between DNA methylation, histone modifications, and small interfering RNAs in the control of cell development and carcinogenesis. In this review, we summarize the recent studies in DNA methylation primarily focusing on the interplay between different epigenetic modifications and their potential role in gene silencing in development and disease. Although the molecular mechanisms involved in the epigenetic crosstalk are not fully understood, unraveling their precise regulation is important not only for understanding the underpinnings of cellular development and cancer, but also for the design of clinically relevant and efficient therapeutics using stem cells and anticancer drugs that target tumor initiating cells.

                Author and article information

                J Cell Mol Med
                J. Cell. Mol. Med
                Journal of Cellular and Molecular Medicine
                John Wiley and Sons Inc. (Hoboken )
                01 October 2019
                December 2019
                : 23
                : 12 ( doiID: 10.1111/jcmm.v23.12 )
                : 8381-8391
                [ 1 ] International Peace Maternity and Child Health Hospital School of Medicine, Shanghai Jiao Tong University Shanghai China
                [ 2 ] Shanghai Key Laboratory of Embryo Origianl Diseases Shanghai China
                [ 3 ] Shanghai Municipal Key Clinical Specialty Shanghai China
                Author notes
                [* ] Correspondence

                Hong Xu and Junyu Zhang, School of Medicine, International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University, No. 910, Heng‐Shan Road, Xu‐Hui Qu, Shanghai 200030, China.

                Emails: xuhong1168@ 123456126.com (HX); junyuzhang@ 123456hotmail.com (JZ)

                © 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                Page count
                Figures: 6, Tables: 1, Pages: 11, Words: 6030
                Funded by: National Natural Science Foundation of China
                Award ID: 81771551
                Award ID: 81501276
                Award ID: 81401219
                Funded by: Shanghai Municipal Commission of Science and Technology Program
                Award ID: 19ZR1462300
                Award ID: 17411972800
                Award ID: 15411966700
                Funded by: Shanghai Municipal Commission of Health and Family Planning
                Award ID: 20154Y0039
                Funded by: Municipal Human Resources Development Program for Outstanding Young Talents in Medical and Health Sciences in Shanghai
                Award ID: 2018YQ39
                Funded by: Shanghai Shenkang Hospital Development Center Clinical Science and Technology Innovation Project
                Award ID: SHDC12017123
                Funded by: Combined Engineering and Medical Project of Shanghai Jiao Tong University
                Award ID: YG2015MS41
                Award ID: YG2017MS39
                Original Article
                Original Articles
                Custom metadata
                December 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.7.1 mode:remove_FC converted:12.11.2019

                Molecular medicine

                adenomyosis, c/ebpβ, dna methylation, eutopic endometrium, rna sequencing


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