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The Molecular Mechanism of Gastrointestinal Malignancies: The Path from Genomic Alterations to Tumor Aggressiveness

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (11 June 2021) | Viewed by 3214

Special Issue Editor

Special Issue Information

Dear Colleagues,

Gastrointestinal (GI) malignancies comprise a group of cancer types, divided by primary site and clinical characteristics, but often sharing similar driving mechanisms. Better stratification and understanding the molecular events that drive these tumors is critical in order to inhibit their development, growth and metastatic spread. Accumulating genomic data provided invaluable information regarding type and frequency of genomic alterations in GI malignancies. However, the mechanistic roles of these alterations are, in most parts, not well defined.

This issue will focus on personalized approach to GI malignancies. We seek high quality manuscripts describing the role of genomic alterations in mediating tumor aggressiveness and metastases formation; the path from genomic alterations to transcriptomic and metabolomic characteristics and the road to resistance therapy.

We specifically encourage the submission of manuscripts presenting innovative approaches exploiting these data in an attempt to identify novel strategies to inhibit tumor growth and spread and overcome resistance to current therapies.

Prof. Dr. Fabio Grizzi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Genomic alterations 
  • Metastases formation 
  • Transcriptional regulation 
  • Tumor metabolism 
  • Targeted therapy 
  • Acquired resistance

Published Papers (1 paper)

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Research

18 pages, 3268 KiB  
Article
The Aneugenicity of Ketone Bodies in Colon Epithelial Cells Is Mediated by Microtubule Hyperacetylation and Is Blocked by Resveratrol
by Haruka Sudo and Akira Kubo
Int. J. Mol. Sci. 2021, 22(17), 9397; https://doi.org/10.3390/ijms22179397 - 30 Aug 2021
Cited by 3 | Viewed by 2664
Abstract
Diabetes mellitus (DM) is considered to be associated with an increased risk of colorectal cancer. Recent studies have also revealed that tubulin hyperacetylation is caused by a diabetic status and we have reported previously that, under microtubule hyperacetylation, a microtubule severing protein, katanin-like [...] Read more.
Diabetes mellitus (DM) is considered to be associated with an increased risk of colorectal cancer. Recent studies have also revealed that tubulin hyperacetylation is caused by a diabetic status and we have reported previously that, under microtubule hyperacetylation, a microtubule severing protein, katanin-like (KL) 1, is upregulated and contributes to tumorigenesis. To further explore this phenomenon, we tested the effects of the ketone bodies, acetoacetate and β-hydroxybutyrate, in colon and fibroblast cells. Both induced microtubule hyperacetylation that responded differently to a histone deacetylase 3 knockdown. These two ketone bodies also generated intracellular reactive oxygen species (ROS) and hyperacetylation was commonly inhibited by ROS inhibitors. In a human fibroblast-based microtubule sensitivity test, only the KL1 human katanin family member showed activation by both ketone bodies. In primary cultured colon epithelial cells, these ketone bodies reduced the tau protein level and induced KL1- and α-tubulin acetyltransferase 1 (ATAT1)-dependent micronucleation. Resveratrol, known for its tumor preventive and tubulin deacetylation effects, inhibited this micronucleation. Our current data thus suggest that the microtubule hyperacetylation induced by ketone bodies may be a causal factor linking DM to colorectal carcinogenesis and may also represent an adverse effect of them that needs to be controlled if they are used as therapeutics. Full article
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