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A cohesin-loading factor (NIPBL) is one of important regulatory factors in the maintenance of 3D genome organization and function, by interacting with a large number of factors, e.g. cohesion, CCCTC-binding factor (CTCF) or cohesin complex component. The present article overviews the critical and regulatory roles of NIBPL in cohesion loading on chromotin and in gene expression and transcriptional signaling. We explore molecular mechanisms by which NIPBL recruits endogenous histone deacetylase (HDAC) to induce histone deacetylation and influence multi-dimensions of genome, through which NIPBL “hop” movement in chromatin regulates gene expression and alters genome folding. NIPBL regulates the process of CTCF and cohesion into chromatin loops and topologically associated domains, binding of cohesion and H3K4mes3 through interaction among promoters and enhancers. HP1 recruits NIPBL to DNA damage site through RNF8/RNF168 ubiquitylation pathway. NIPBL contributes to regulation of genome-controlled gene expression through the influence of cohesin in chromosome structure. NIPBL interacts with cohesin and then increases transcriptional activities of REC8 promoter, leading to up-regulation of gene expression. NIPBL movement among chromosomal loops regulates gene expression through dynamic alterations of genome organization. Thus, we expect a new and deep insight to understand dynamics of chromosome and explore potential strategies of therapiesc on basis of NIPBL.

Lung cancer is a leading cause of cancer‐related deaths with an increasing incidence and poor prognoses. To further understand the regulatory mechanisms of lipidomic profiles in lung cancer subtypes, we measure the profiles of plasma lipidome between health and patients with lung cancer or among patients with squamous cell carcinomas, adenocarcinoma or small cell lung cancer and to correct lipidomic and genomic profiles of lipid‐associated enzymes and proteins by integrating the data of large‐scale genome screening. Our studies demonstrated that circulating levels of PS and lysoPS significantly increased, while lysoPE and PE decreased in patients with lung cancer. Our data indicate that lung cancer‐specific and subtype‐specific lipidomics in the circulation are important to understand mechanisms of systemic metabolisms and identify diagnostic biomarkers and therapeutic targets. The carbon atoms, dual bonds or isomerism in the lipid molecule may play important roles in lung cancer cell differentiations and development. This is the first try to integrate lipidomic data with lipid protein‐associated genomic expression among lung cancer subtypes as the part of clinical trans‐omics. We found that a large number of lipid protein‐associated genes significantly change among cancer subtypes, with correlations with altered species and spatial structures of lipid metabolites.

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Most researchers focused on methylation of genomic DNA, while methylation of mitochondrial DNA (mtDNA) is rarely tauched, and there is still controversy about the existence of mtDNA methylation. The study of cytosine methylation in mtDNA is limited. The mtDNA was recently found to exist CpG hypomethylation, and more studies provided evidence that mtDNA methylation plays an important role in mitochondrial gene regulation. In present review, we will overview recent studies of mitochondrial DNA methylation and potential influencing factors in diseases that are involved in mtDNA methylation. Thus, the further studies on mtDNA methylation will provide more evidence to explain the mechanism of mtDNA methylation and an advantageous approach for human clinical diagnosis and prevention.

Most researchers focused on methylation of genomic DNA, while methylation of mitochondrial DNA (mtDNA) is rarely tauched, and there is still controversy about the existence of mtDNA methylation. The study of cytosine methylation in mtDNA is limited. The mtDNA was recently found to exist CpG hypomethylation, and more studies provided evidence that mtDNA methylation plays an important role in mitochondrial gene regulation. In present review, we will overview recent studies of mitochondrial DNA methylation and potential influencing factors in diseases that are involved in mtDNA methylation. Thus, the further studies on mtDNA methylation will provide more evidence to explain the mechanism of mtDNA methylation and an advantageous approach for human clinical diagnosis and prevention.

Genetic variations in COPD and lung cancer may be one of the molecular mechanisms responsible for COPD-lung cancer transformation. The present review highlights main genetic variations co-existed in COPD and lung cancer and integrates the varied genes into four molecular mechanisms, e.g. activated cell proliferation pathway, tumor suppressor and DNA repair gene dysfunction, chronic inflammatory microenvironment, and impaired immune response, by which COPD epithelial cells may be transformed into tumorigenic status. We call special attention to further investigate the transformation from COPD to lung cancer and understand the exact molecular mechanisms, to prevent and reduce the increased incidence of COPD and lung cancer. We call direct evidence to show the existence of COPD-lung cancer transformation, since current evidence to support the transformation from COPD to lung cancer is the co-existence of selected genes and proteins in both. We should furthermore explore and understand the homogeneity and heterogeneity of gene mutation, epigenetics, sequencing, and function between COPD and lung cancer. The defining and understanding of COPD-lung cancer transformation will provide new diagnostic and therapeutic biomarkers as a new milestone to prevent and treat lung cancer.