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Core pluripotency factors promote glycolysis of human embryonic stem cells by activating GLUT1 enhancer

Protein & Cell 2019年第9期10卷 668-680页

作者： Lili Yu Kai-yuan Ji Jian Zhang Yanxia Xu Yue Ying Taoyi Mai Shuxiang Xu Qian-bing Zhang Kai-tai Yao Yang Xu Cancer Research Institute Guan gdong Provin cial Key Laboratory of Cancer Immuno therapySchool of Basic Medical SciencesSouthern Medical UniversityGuangzhou 510515China The Eighth Affiliated Hospital Sun Yat-sen UniversityShenzhen 518033GuangdongChina

Human embryonic stem cells (hESCs) depend on glycolysis for energy and substrates for biosynthesis. To understand the mechanisms governing the metabolism of hESCs, we investigated the transcriptional regulation of glucose transporter 1 (GLUT1, SLC2A1), a key glycolytic gene to maintain pluripotency. By combining the genome-wide data of bin ding sites of the core pluripotency factors (SOX2, OCT4, NANOG, denoted SON), chromosomal interaction and histone modification in hESCs, we identified a potential enhancer of the GLUT1 gene in hESCs, de noted GLUT1 enhancer (GE) element GE interacts with the promoter of GLUT1, and the deletion of GE significantly reduces the expression of GLUT1, glucose uptake and glycolysis of hESCs, confirming that GE is an enhancer of GLUT1 in hESCs. In addition, the mutation of SON binding motifs within GE reduced the expression of GLUT1 as well as the interaction between GE and GLUT1 promoter, indicating that the binding of SON to GE is important for its activity. Therefore, SON promotes glucose uptake and glycolysis in hESCs by inducing GLUT1 expression through directly activating the enhancer of GLUT1.

关键词： human embryonic stem cell pluripotency factors, metabolism Glutl enhancer promoter epigenetics, chromosome interaction

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Detection and characterization of regulatory elements using probabilistic conditional random field and hidden Markov models

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Chinese Journal of Cancer 2013年第4期32卷 186-194页

作者： Hongyan Wang Xiaobo Zhou Department of Radiology the Methodist Hospital Research Institute Department of Radiology Weill Cornell Medical College

By altering the electrostatic charge of histones or providing binding sites to protein recognition molecules, Chromatin marks have been proposed to regulate gene expression, a property that has motivated researchers to link these marks to cis-regulatory elements. With the help of next generation sequencing technologies, we can now correlate one specific chromatin mark with regulatory elements (e.g. enhancers or promoters) and also build tools, such as hidden Markov models, to gain insight into mark combinations. However, hidden Markov models have limitation for their character of generative models and assume that a current observation depends only on a current hidden state in the chain. Here, we employed two graphical probabilistic models, namely the linear conditional random field model and multivariate hidden Markov model, to mark gene regions with different states based on recurrent and spatially coherent character of these eight marks. Both models revealed chromatin states that may correspond to enhancers and promoters, transcribed regions, transcriptional elongation, and low-signal regions. We also found that the linear conditional random field model was more effective than the hidden Markov model in recognizing regulatory elements, such as promoter-, enhancer-, and transcriptional elongation-associated regions, which gives us a better choice.

关键词： epigenetics, histone modification, conditional random field, regulatory elements

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Carcinogenic efects of circadian disruption: an epigenetic viewpoint

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Chinese Journal of Cancer 2015年第9期34卷 1-9页

作者： Abbas Salavaty Department of Genetics Faculty of ScienceShahid Chamran University of Ahvaz

Circadian rhythms refer to the endogenous rhythms that are generated to synchronize physiology and behavior with 24-h environmental cues. These rhythms are regulated by both external cues and molecular clock mechanisms in almost all cells. Disruption of circadian rhythms, which is called circadian disruption, afects many biological processes within the body and results in diferent long-term diseases, including cancer. Circadian regulatory pathways result in rhythmic epigenetic modiications and the formation of circadian epigenomes. Aberrant epigenetic modiications, such as hypermethylation, due to circadian disruption may be involved in the transformation of normal cells into cancer cells. Several studies have indicated an epigenetic basis for the carcinogenic efects of circadian disruption. In this review, I irst discuss some of the circadian genes and regulatory proteins. Then, I summarize the current evidence related to the epigenetic modiications that result in circadian disruption. In addition, I explain the carcinogenic efects of circadian disruption and highlight its potential role in diferent human cancers using an epigenetic viewpoint. Finally, the importance of chronotherapy in cancer treatment is highlighted.

关键词： Cancer, epigenetics, Circadian rhythms, Circadian disruption, Chronotherapy

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