Mitotic Functions and Characters of KIF11 in Cancers

Introduction: Esophageal chemical burns often occur through accidental or intentional oral consumption of chemical agents and lead to severe complications such as esophageal stricture, acute perforation, and even death. Esophageal squamous cell carcinoma (ESCC) is a squamous epithelium tumor that lines the normal esophagus. Additionally, adenocarcinomas are tumors located at the interface between the distal esophagus and the proximal Gastric and divided into esophageal adenocarcinoma (EAC) and gastric-cardia adenocarcinoma. Various conditions, such as chemical burns, are considered risk factors in the disease’s pathogenesis. In the in-silico study, the authors aim to present the relationship between chemical burns and esophageal cancer by analyzing bioinformatics genetic data. Methods: The proper gene set was extracted using the “GEO” database. The string web tool was utilized to form the gene-interaction network. Gephi and Cytoscape software were applied to achieve network analysis. Results: According to in-silico data, 26 genes, including NCAPH, DLGAP5, CCNB1, KIF11, KIAA0101, CDCA5, BIRC5, NUF2, BUB1B, RRM2, TTK, CDC20, NUSAP1, CCNB2, CCNA2, MELK, TPX2, PRC1, KIF4A, CENPF, TOP2A, CDK1, ASPM, CEP55, BUB1, KIF20A were extracted that can be regarded as the most critical shared genes between chemical burns and esophageal cancer. Conclusion: In sum, esophageal chemical burns can be related to the occurrence of esophageal cancer. Moreover, esophageal chemical burn is an external factor that upregulates present genes and can be regarded as a worsening prognosis or risk factor for esophageal cancer.

show abstract

Age-Dependent Maturation and Rejuvenation of the Neural 3D Chromatin Interactome in Enriched Environments

Gancedo-Verdejo,

Urdinguio,

Tejedor

et al. 2024

Preprint

View full text Add to dashboard Cite

Aging is a multifactorial biological process resulting in physiological and cellular decline. However, our understanding of age-related changes in 3D genome organization and the effect of external interventions on this process, remains limited. Here we describe alterations in the landscape of the 3D chromatin interactome upon aging, utilizing the low input Promoter Capture Hi-C (liCHi-C) technique with hippocampal neurons. We integrated liCHi-C data with RNA-seq data to identify functional implications. Furthermore, we assessed the effect of exposure to environmental enrichment (EE). Remarkably, our results demonstrated an age-dependent modulation of promoter interactions and expression with EE, with aging-like changes induced in young mice upon EE, likely associated with early brain maturation; while age-related alterations were reverted in old mice, leading to a partial rejuvenation of aged mouse hippocampi. These findings revealed a dynamic behaviour of the neuronal 3D chromatin structure over time, which can be modulated by external interventions.

show abstract

Mitotic Functions and Characters of KIF11 in Cancers

Cited by 5 publications

References 211 publications

The role of kinesin superfamily proteins in hepatocellular carcinoma

The role of kinesin superfamily proteins in hepatocellular carcinoma

Esophageal chemical burns as a risk factor for esophageal malignancies: in-silico analyses-experimental research

Age-Dependent Maturation and Rejuvenation of the Neural 3D Chromatin Interactome in Enriched Environments

Contact Info

Product

Resources

About