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Cancer Genomics
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Cancer Genomics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 September 2024 | Viewed by 4458

Special Issue Editors

Dr. Ricardo Armisén

E-Mail Website1 Website2
Guest Editor
Facultad de Medicina Clínica Alemana, Universidad del Desarrollo, Concepcin, Chile
Interests: RNA biology; cancer functional genomics; precision medicine; molecular diagnostics
Dr. Hector R. Contreras

E-Mail Website
Guest Editor
Laboratory of Cellular and Molecular Oncology, Department of Basic and Clinical Oncology, Faculty of Medicine, University de Chile, Santiago 8380453, Chile
Interests: epithelial–mesenchymal transition; cancer stem cell; prostate cancer; colon cancer; breast cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

During the development and progression of cancer, neoplastic cells acquire a series of genetic changes that result in drastic modifications both in how the cell responds to its environment and in the cell dynamics itself. Advancements in genomic technologies and next-generation sequencing have produced a wealth of information and provided substantial insights into the pathogenesis of diseases. Especially in cancer, these tools have been exceptionally useful for identifying novel signal transduction pathways, with a great potential for the discovery of new biomarkers and therapeutic targets. However, the translation of these findings into a breakthrough in the understanding of cancer biology and the care of cancer patients remains a major challenge.

This Special Issue highlights novel findings in cancer genomics arising from the combined use of computational tools, high-throughput sequencing technology, bioinformatics, cell biology and translational research to understand cancer biology, from genomics to cell signaling and from disease models to actual patients. Translational efforts to make the knowledge of cellular and molecular biology of cancer useful for patients with cancer, and research performed in understudied specific cancer patients, are of special interest.

Dr. Ricardo Armisén
Dr. Hector R. Contreras
Guest Editors

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

  • precision oncology
  • cancer genomics
  • personalized medicine
  • mutagenesis
  • molecular epidemiology

Published Papers (3 papers)

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Research

18 pages, 8512 KiB  
Article
Stratification of Colorectal Patients Based on Survival Analysis Shows the Value of Consensus Molecular Subtypes and Reveals the CBLL1 Gene as a Biomarker of CMS2 Tumours
by Gloria Alfonsín, Alberto Berral-González, Andrea Rodríguez-Alonso, Macarena Quiroga, Javier De Las Rivas and Angélica Figueroa
Int. J. Mol. Sci. 2024, 25(3), 1919; https://doi.org/10.3390/ijms25031919 - 5 Feb 2024
Viewed by 968
Abstract
The consensus molecular subtypes (CMSs) classification of colorectal cancer (CRC) is a system for patient stratification that can be potentially applied to therapeutic decisions. Hakai (CBLL1) is an E3 ubiquitin–ligase that induces the ubiquitination and degradation of E-cadherin, inducing epithelial-to-mesenchymal transition (EMT), tumour [...] Read more.
The consensus molecular subtypes (CMSs) classification of colorectal cancer (CRC) is a system for patient stratification that can be potentially applied to therapeutic decisions. Hakai (CBLL1) is an E3 ubiquitin–ligase that induces the ubiquitination and degradation of E-cadherin, inducing epithelial-to-mesenchymal transition (EMT), tumour progression and metastasis. Using bioinformatic methods, we have analysed CBLL1 expression on a large integrated cohort of primary tumour samples from CRC patients. The cohort included survival data and was divided into consensus molecular subtypes. Colon cancer tumourspheres were used to analyse the expression of stem cancer cells markers via RT-PCR and Western blotting. We show that CBLL1 gene expression is specifically associated with canonical subtype CMS2. WNT target genes LGR5 and c-MYC show a similar association with CMS2 as CBLL1. These mRNA levels are highly upregulated in cancer tumourspheres, while CBLL1 silencing shows a clear reduction in tumoursphere size and in stem cell biomarkers. Importantly, CMS2 patients with high CBLL1 expression displayed worse overall survival (OS), which is similar to that associated with CMS4 tumours. Our findings reveal CBLL1 as a specific biomarker for CMS2 and the potential of using CMS2 with high CBLL1 expression to stratify patients with poor OS. Full article
(This article belongs to the Special Issue Cancer Genomics)
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15 pages, 3011 KiB  
Article
miR-195-5p as Regulator of γ-Catenin and Desmosome Junctions in Colorectal Cancer
by Emanuele Piccinno, Viviana Scalavino, Raffaele Armentano, Gianluigi Giannelli and Grazia Serino
Int. J. Mol. Sci. 2023, 24(23), 17084; https://doi.org/10.3390/ijms242317084 - 3 Dec 2023
Cited by 2 | Viewed by 1132
Abstract
Desmosomes play a key role in the regulation of cell adhesion and signaling. Dysregulation of the desmosome complex is associated with the loss of epithelial cell polarity and disorganized tissue architecture typical of colorectal cancer (CRC). The aim of this study was to [...] Read more.
Desmosomes play a key role in the regulation of cell adhesion and signaling. Dysregulation of the desmosome complex is associated with the loss of epithelial cell polarity and disorganized tissue architecture typical of colorectal cancer (CRC). The aim of this study was to investigate and characterize the effect of miR-195-5p on desmosomal junction regulation in CRC. In detail, we proposed to investigate the deregulation of miR-195-5p and JUP, a gene target that encodes a desmosome component in CRC patients. JUP closely interacts with desmosomal cadherins, and downstream, it regulates several intracellular transduction factors. We restored the miR-195-5p levels by transient transfection in colonic epithelial cells to examine the effects of miR-195-5p on JUP mRNA and protein expression. The JUP regulation by miR-195-5p, in turn, determined a modulation of desmosome cadherins (Desmoglein 2 and Desmocollin 2). Furthermore, we focused on whether the miR-195-5p gain of function was also able to modulate the expression of key components of Wnt signaling, such as NLK, LEF1 and Cyclin D1. In conclusion, we have identified a novel mechanism controlled by miR-195-5p in the regulation of adhesive junctions, suggesting its potential clinical relevance for future miRNA-based therapy in CRC. Full article
(This article belongs to the Special Issue Cancer Genomics)
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17 pages, 5378 KiB  
Article
Firing of Replication Origins Is Disturbed by a CDK4/6 Inhibitor in a pRb-Independent Manner
by Su-Jung Kim, Chrystelle Maric, Lina-Marie Briu, Fabien Fauchereau, Giuseppe Baldacci, Michelle Debatisse, Stéphane Koundrioukoff and Jean-Charles Cadoret
Int. J. Mol. Sci. 2023, 24(13), 10629; https://doi.org/10.3390/ijms241310629 - 25 Jun 2023
Viewed by 1525
Abstract
Over the last decade, CDK4/6 inhibitors (palbociclib, ribociclib and abemaciclib) have emerged as promising anticancer drugs. Numerous studies have demonstrated that CDK4/6 inhibitors efficiently block the pRb-E2F pathway and induce cell cycle arrest in pRb-proficient cells. Based on these studies, the inhibitors have [...] Read more.
Over the last decade, CDK4/6 inhibitors (palbociclib, ribociclib and abemaciclib) have emerged as promising anticancer drugs. Numerous studies have demonstrated that CDK4/6 inhibitors efficiently block the pRb-E2F pathway and induce cell cycle arrest in pRb-proficient cells. Based on these studies, the inhibitors have been approved by the FDA for treatment of advanced hormonal receptor (HR) positive breast cancers in combination with hormonal therapy. However, some evidence has recently shown unexpected effects of the inhibitors, underlining a need to characterize the effects of CDK4/6 inhibitors beyond pRb. Our study demonstrates how palbociclib impairs origin firing in the DNA replication process in pRb-deficient cell lines. Strikingly, despite the absence of pRb, cells treated with palbociclib synthesize less DNA while showing no cell cycle arrest. Furthermore, this CDK4/6 inhibitor treatment disturbs the temporal program of DNA replication and reduces the density of replication forks. Cells treated with palbociclib show a defect in the loading of the Pre-initiation complex (Pre-IC) proteins on chromatin, indicating a reduced initiation of DNA replication. Our findings highlight hidden effects of palbociclib on the dynamics of DNA replication and of its cytotoxic consequences on cell viability in the absence of pRb. This study provides a potential therapeutic application of palbociclib in combination with other drugs to target genomic instability in pRB-deficient cancers. Full article
(This article belongs to the Special Issue Cancer Genomics)
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