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Cells
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Molecular and Cellular Mechanisms of Cancers: Colorectal Cancer
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Molecular and Cellular Mechanisms of Cancers: Colorectal Cancer

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 January 2020) | Viewed by 17572

Special Issue Editors

Dr. Peter J. K. Kuppen

E-Mail Website
Guest Editor
Department of Surgery, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands
Interests: colorectal cancer; tumor-immmune interactions; cancer genetics and epigenetics; immunotherapy; biomarkers
Special Issues, Collections and Topics in MDPI journals
Dr. Luca Roncucci

E-Mail Website
Guest Editor
Department of Medical and Surgical Sciences, University of Modena and Reggio Emilia, I-41125 Modena, Italy
Interests: colorectal cancer; colorectal carcinogenesis; inflammation and metabolic risk factors for cancer; hereditary colorectal cancer; colorectal adenomas; aberrant crypt foci
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

With over 700,000 deaths world-wide annually, colorectal cancer remains a large societal burden. Our knowledge of the underlying biology of colorectal tumor formation is impressive, but still, we are not able to efficiently fight this disease. Recent insights are that we should not only focus on biological processes that take place in the tumor cell itself, steered by both genetic and epigenetic events, but also on the response of the environment. This Special Issue aims to focus on that environmental interaction and its steering processes, and on the mechanisms involved in the early and later steps of colorectal cancer development. Finally, we will discuss the conditions that may lead to a better clinical approach to colorectal cancer.

We very much look forward to your contributions.

Prof. Peter Kuppen
Prof. Luca Roncucci
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • colorectal cancer
  • tumor microenvironment
  • tumor host response
  • tumor genetics and epigenetics
  • colorectal carcinogenesis
  • colorectal cancer prevention

Published Papers (4 papers)

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Research

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12 pages, 1367 KiB  
Article
Analysis of Killer Immunoglobulin-Like Receptor Genes in Colorectal Cancer
by Roberto Diaz-Peña, Patricia Mondelo-Macía, Antonio José Molina de la Torre, Rebeca Sanz-Pamplona, Víctor Moreno and Vicente Martín
Cells 2020, 9(2), 514; https://doi.org/10.3390/cells9020514 - 24 Feb 2020
Cited by 6 | Viewed by 2875
Abstract
Natural killer cells (NK cells) play a major role in the immune response to cancer. An important element of NK target recognition is the binding of human leucocyte antigen (HLA) class I molecules by killer immunoglobulin-like receptors (KIRs). Colorectal carcinoma (CRC) is one [...] Read more.
Natural killer cells (NK cells) play a major role in the immune response to cancer. An important element of NK target recognition is the binding of human leucocyte antigen (HLA) class I molecules by killer immunoglobulin-like receptors (KIRs). Colorectal carcinoma (CRC) is one of the most common types of inflammation-based cancer. The purpose of the present study was to investigate the presence of KIR genes and HLA class I and II alleles in 1074 CRC patients and 1272 controls. We imputed data from single-nucleotide polymorphism (SNP) Illumina OncoArray to identify associations at HLA (HLA–A, B, C, DPB1, DQA1, DQB1, and DRB1) and KIRs (HIBAG and KIR*IMP, respectively). For association analysis, we used PLINK (v1.9), the PyHLA software, and R version 3.4.0. Only three SNP markers showed suggestive associations (p < 10−3; rs16896742, rs28367832, and rs9277952). The frequency of KIR2DS3 was significantly increased in the CRC patients compared to healthy controls (p < 0.005). Our results suggest that the implication of NK cells in CRC may not act through allele combinations in KIR and HLA genes. Much larger studies in ethnically homogeneous populations are needed to rule out the possible role of allelic combinations in KIR and HLA genes in CRC risk. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Colorectal Cancer)
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Review

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18 pages, 1281 KiB  
Review
Functions and Implications of Autophagy in Colon Cancer
by Samantha N Devenport and Yatrik M Shah
Cells 2019, 8(11), 1349; https://doi.org/10.3390/cells8111349 - 30 Oct 2019
Cited by 49 | Viewed by 5245
Abstract
Autophagy is an essential function to breakdown cellular proteins and organelles to recycle for new nutrient building blocks. In colorectal cancer, the importance of autophagy is becoming widely recognized as it demonstrates both pro- and anti-tumorigenic functions. In colon cancer, cell autonomous and [...] Read more.
Autophagy is an essential function to breakdown cellular proteins and organelles to recycle for new nutrient building blocks. In colorectal cancer, the importance of autophagy is becoming widely recognized as it demonstrates both pro- and anti-tumorigenic functions. In colon cancer, cell autonomous and non-autonomous roles for autophagy are essential in growth and progression. However, the mechanisms downstream of autophagy (to reduce or enhance tumor growth) are not well known. Additionally, the signals that activate and coordinate autophagy for tumor cell growth and survival are not clear. Here, we highlight the context- and cargo-dependent role of autophagy in proliferation, cell death, and cargo breakdown. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Colorectal Cancer)
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21 pages, 1319 KiB  
Review
Inhibition of Caspase-2 Translation by the mRNA Binding Protein HuR: A Novel Path of Therapy Resistance in Colon Carcinoma Cells?
by Wolfgang Eberhardt, Usman Nasrullah and Kristina Haeussler
Cells 2019, 8(8), 797; https://doi.org/10.3390/cells8080797 - 30 Jul 2019
Cited by 13 | Viewed by 4185
Abstract
An increased expression and cytoplasmic abundance of the ubiquitous RNA binding protein human antigen R (HuR) is critically implicated in the dysregulated control of post-transcriptional gene expression during colorectal cancer development and is frequently associated with a high grade of malignancy and therapy [...] Read more.
An increased expression and cytoplasmic abundance of the ubiquitous RNA binding protein human antigen R (HuR) is critically implicated in the dysregulated control of post-transcriptional gene expression during colorectal cancer development and is frequently associated with a high grade of malignancy and therapy resistance. Regardless of the fact that HuR elicits a broad cell survival program by increasing the stability of mRNAs coding for prominent anti-apoptotic factors, recent data suggest that HuR is critically involved in the regulation of translation, particularly, in the internal ribosome entry site (IRES) controlled translation of cell death regulatory proteins. Accordingly, data from human colon carcinoma cells revealed that HuR maintains constitutively reduced protein and activity levels of caspase-2 through negative interference with IRES-mediated translation. This review covers recent advances in the understanding of mechanisms underlying HuR’s modulatory activity on IRES-triggered translation. With respect to the unique regulatory features of caspase-2 and its multiple roles (e.g., in DNA-damage-induced apoptosis, cell cycle regulation and maintenance of genomic stability), the pathophysiological consequences of negative caspase-2 regulation by HuR and its impact on therapy resistance of colorectal cancers will be discussed in detail. The negative HuR-caspase-2 axis may offer a novel target for tumor sensitizing therapies. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Colorectal Cancer)
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17 pages, 949 KiB  
Review
Selected Aspects of Chemoresistance Mechanisms in Colorectal Carcinoma—A Focus on Epithelial-to-Mesenchymal Transition, Autophagy, and Apoptosis
by Veronika Skarkova, Vera Kralova, Barbora Vitovcova and Emil Rudolf
Cells 2019, 8(3), 234; https://doi.org/10.3390/cells8030234 - 12 Mar 2019
Cited by 47 | Viewed by 4417
Abstract
Chemoresistance has been found in all malignant tumors including colorectal carcinoma (CRC). Nowadays chemoresistance is understood as a major reason for therapy failure, with consequent tumor growth and spreading leading ultimately to the patient’s premature death. The chemotherapy-related resistance of malignant colonocytes may [...] Read more.
Chemoresistance has been found in all malignant tumors including colorectal carcinoma (CRC). Nowadays chemoresistance is understood as a major reason for therapy failure, with consequent tumor growth and spreading leading ultimately to the patient’s premature death. The chemotherapy-related resistance of malignant colonocytes may be manifested in diverse mechanisms that may exist both prior to the onset of the therapy or after it. The ultimate function of this chemoresistance is to ensure the survival of malignant cells through continuing adaptation within an organism, therefore, the nature and spectrum of cell-survival strategies in CRC represent a highly significant target of scientific inquiry. Among these survival strategies employed by CRC cells, three unique but significantly linked phenomena stand out—epithelial-to-mesenchymal transition (EMT), autophagy, and cell death. In this mini-review, current knowledge concerning all three mechanisms including their emergence, timeline, regulation, and mutual relationships will be presented and discussed. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Colorectal Cancer)
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