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RNA Sequencing Data Research on Ageing and Age-Related Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 996

Special Issue Editors


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Guest Editor
Reta Lila Weston Research Laboratories, Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK
Interests: brain; Alzheimer’s disease

Special Issue Information

Dear Colleagues,

Ageing is a complex process influenced by genetic and epigenetic regulation, post-translational regulation, metabolic regulation, lifestyle, and many other elements. New research methods, drugs, and clinical treatments are emerging, offering opportunities to reveal the mechanisms of ageing and the prevention or treatment of ageing-related diseases.

We have previously studied ageing gene expression changes in the human brain via analyses of exon microarrays from 1234 post mortem brains of individuals who passed away between the ages of 16 and over 100 (UK Brain Bank). We found cell-type-specific gene expression changes and, in particular, a decrease in neuronal gene expression and an increase in microglial genes. We also quantified neurons and oligodendrocytes through machine learning and image analyses and detected an increase in the number of large neurons and a decrease in oligodendrocytes in old brain samples compared to young ones. RNA-Seq allows for the detailed analysis of patients compared to control post mortem brain samples using statistical/bioinformatic analyses. Ageing is a major risk factor for Alzheimer’s disease, the second most frequent neurodegenerative disease worldwide. Future statistical/bioinformatic analyses may focus on specific brain cell types (such as neurons, endothelial cells, oligodendrocytes microglia, and astrocytes).

The proposed topics include, but are not limited to, the following:

  • Neurodegenerative diseases;
  • The role of neuroinflammation in the development of ageing;
  • Ageing gene expression;
  • Molecular biomarkers of ageing;
  • Experimental models of ageing.

Dr. Lilach Soreq
Prof. Dr. John Hardy
Guest Editors

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Keywords

  • ageing
  • bioinformatics
  • Alzheimer’s disease
  • Parkinson’s disease
  • RNA-Seq

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Published Papers (1 paper)

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Research

15 pages, 3346 KiB  
Article
Downregulation of Splicing Factor PTBP1 Curtails FBXO5 Expression to Promote Cellular Senescence in Lung Adenocarcinoma
by Haoyu Li, Xiaoxiao Sun, Yuanyuan Lv, Gang Wei, Ting Ni, Wenxin Qin, Haojie Jin and Qi Jia
Curr. Issues Mol. Biol. 2024, 46(7), 7730-7744; https://doi.org/10.3390/cimb46070458 - 19 Jul 2024
Viewed by 724
Abstract
Polypyrimidine tract-binding protein 1 (PTBP1) plays an essential role in splicing and post-transcriptional regulation. Moreover, PTBP1 has been implicated as a causal factor in tumorigenesis. However, the involvement of PTBP1 in cellular senescence, a key biological process in aging and cancer [...] Read more.
Polypyrimidine tract-binding protein 1 (PTBP1) plays an essential role in splicing and post-transcriptional regulation. Moreover, PTBP1 has been implicated as a causal factor in tumorigenesis. However, the involvement of PTBP1 in cellular senescence, a key biological process in aging and cancer suppression, remains to be clarified. Here, it is shown that PTBP1 is associated with the facilitation of tumor growth and the prognosis in lung adenocarcinoma (LUAD). PTBP1 exhibited significantly increased expression in various cancer types including LUAD and showed consistently decreased expression in multiple cellular senescence models. Suppression of PTBP1 induced cellular senescence in LUAD cells. In terms of molecular mechanisms, the silencing of PTBP1 enhanced the skipping of exon 3 in F-box protein 5 (FBXO5), resulting in the generation of a less stable RNA splice variant, FBXO5-S, which subsequently reduces the overall FBXO5 expression. Additionally, downregulation of FBXO5 was found to induce senescence in LUAD. Collectively, these findings illustrate that PTBP1 possesses an oncogenic function in LUAD through inhibiting senescence, and that targeting aberrant splicing mediated by PTBP1 has therapeutic potential in cancer treatment. Full article
(This article belongs to the Special Issue RNA Sequencing Data Research on Ageing and Age-Related Diseases)
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