Relationship between High Expression of Kaiso Protein and Poor Prognosis of Lung Cancer and the Regulation Mechanism of Malignant Phenotype of Lung Cancer Cells

In this study, Kaiso was discovered to be a unique member of the POZ-zinc fingers family of transcription factors, which has been implicated in the genesis and progression of cancer. Although there is still some debate, Kaiso is believed to be implicated in the development of human cancer. It should be noted that there is minimal evidence available on the therapeutic relevance of nuclear Kaiso in lung cancer in humans. Histone or DNA modifications that control gene activity outside of the underlying sequence are examples of epigenetic alternations. Epigenetic alterations are heritable but reversible. Human illness, such as lung cancer, is often related to epigenetic dysregulation. In preclinical and clinical studies, epigenetic-targeted therapy has shown significant therapeutic promise for solid tumours and has been used in the treatment of haematological malignancies using different medicines targeting epigenetic regulators. It is important to note that the abnormal activities of Kaiso enzymes in tumour growth are summarised below and the development of inhibitors or medicines targeting epigenetic enzyme regulation is highlighted.

Molecular Basis of the Function of Transcriptional Enhancers

Transcriptional enhancers are major genomic elements that control gene activity in eukaryotes. Recent studies provided deeper insight into the temporal and spatial organization of transcription in the nucleus, the role of non-coding RNAs in the process, and the epigenetic control of gene expression. Thus, multiple molecular details of enhancer functioning were revealed. Here, we describe the recent data and models of molecular organization of enhancer-driven transcription.

Live-cell imaging reveals enhancer-dependent Sox2 transcription in the absence of enhancer proximity

Enhancers are important regulatory elements that can control gene activity across vast genetic distances. However, the underlying nature of this regulation remains obscured because it has been difficult to observe in living cells. Here, we visualize the spatial organization and transcriptional output of the key pluripotency regulator Sox2 and its essential enhancer Sox2 Control Region (SCR) in living embryonic stem cells (ESCs). We find that Sox2 and SCR show no evidence of enhanced spatial proximity and that spatial dynamics of this pair is limited over tens of minutes. Sox2 transcription occurs in short, intermittent bursts in ESCs and, intriguingly, we find this activity demonstrates no association with enhancer proximity, suggesting that direct enhancer-promoter contacts do not drive contemporaneous Sox2 transcription. Our study establishes a framework for interrogation of enhancer function in living cells and supports an unexpected mechanism for enhancer control of Sox2 expression that uncouples transcription from enhancer proximity.

Live-Cell Imaging Reveals Enhancer-dependent Sox2 Transcription in the Absence of Enhancer Proximity

ABSTRACTEnhancers are important regulatory elements that can control gene activity across vast genetic distances. However, the underlying nature of this regulation remains obscured because it has been difficult to observe in living cells. Here, we visualize the spatial organization and transcriptional output of the key pluripotency regulatorSox2and its essential enhancerSox2Control Region (SCR) in living embryonic stem cells (ESCs). We find thatSox2and SCR show no evidence of enhanced spatial proximity and that spatial dynamics of this pair is limited over tens of minutes.Sox2transcription occurs in short, intermittent bursts in ESCs and, intriguingly, we find this activity demonstrates no association with enhancer proximity, suggesting that direct enhancer-promoter contacts do not drive contemporaneousSox2transcription. Our study establishes a framework for interrogation of enhancer function in living cells and supports an unexpected mechanism for enhancer control ofSox2expression that uncouples transcription from enhancer proximity.

The Expanding Mi-2/NuRD Complexes: A Schematic Glance

This mini-review will schematically update the progress of the expanding Mi-2/Nucleosome Remodeling Deacetylase (NuRD) complexes in cancer and in normal development such as stemness, with a focus on mammals and the increasingly popular and powerful model organism Caenorhabditis elegans. The Mi-2/NuRD complexes control gene activity during the development of complex organisms. Every Mi-2/NuRD complex contains many different core polypeptides, which form distinct multifunctional complexes with specific context-dependent regulators. The Mi-2/NuRD complexes have unique ATP-dependent chromatin remodeling, histone deacetylase, demethylase activities and higher order chromatin organization. They can regulate the accessibility of transcription factors or repair proteins to DNA. In this review, we summarize our current knowleges in the composition, interaction and function of the subunits within the Mi-2/NuRD complex, the methodology used for the identification of Mi-2/NuRD complexes, as well as the clinical and therapeutic implications targeting the Mi-2/NuRD subunits.

Studies on the Template Activity of ‘Isolated" Xenopus Erythrocyte Nuclei

The isolation and characterization of nuclei from Xenopus erythrocytes is described. Such nuclei are freely permeable to ions and large molecules. They have an extremely low basal rate of RNA synthesis which can be increased by the addition of Escherichia coli RNA polymerase and by alteration in the ionic strength of the incubation medium within physiological limits. The results are discussed in terms of the mechanisms which control gene activity in these cells.