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Molecular Advances in Colorectal Cancer
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Molecular Advances in Colorectal Cancer

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 (15 April 2023) | Viewed by 13678

Special Issue Editors

Dr. Josefa León

E-Mail Website
Guest Editor
Biosanitary Research Institute, ibs.Granada, 18012 Granada, Spain
Interests: cancer; cancer-stem-like cells; oxidative stress; circadian clock
Special Issues, Collections and Topics in MDPI journals
Dr. María Isabel Rodríguez

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology III and Immunology, University of Granada, Granada, Spain
Interests: cancer; SWI/SNF complex; PARP
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Colorectal cancer (CRC) is one of the most common malignant tumors. Despite the improved prevention and detection of this disease, its prognosis has currently not changed, and more than 50% of patients will develop liver metastases during their disease, which represent the main cause of morbidity and mortality. Local recurrence (LR) at the first site of disease is much less common, constituting 10 to 20% of all relapses. Another important issue in CRC is the intrinsic or acquired resistance to treatments. Great effort has been made to identify patients with unfavourable prognosis that may benefit from adjuvant therapy. However, to date, therapy in CRC is used only if there are metastases. The choice of target agents for colorectal cancer therapy is limited, and their efficiency is not always compelling. Even in patients with similar clinical or pathologic features, their survival outcomes vary. Therefore, the discovery of new molecular markers to improve the prognosis and prediction of the adjuvant treatment regimens that enable personalized cancer therapies are urgently needed.

This Special Issue aims to present the most recent results on the selection of molecular biomarkers in colorectal cancer from basic studies. We welcome original research articles, comprehensive reviews, and novel short communications.

Prof. Dr. Josefa León
Dr. María Isabel Rodríguez
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

  • colorectal cancer
  • CRC
  • bowel cancer
  • colon cancer
  • rectal cancer
  • molecular pathology
  • genetics
  • epigenetics
  • immunotherapy
  • diagnostics
  • therapeutics

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Published Papers (5 papers)

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Research

15 pages, 3530 KiB  
Article
PLA2G12A as a Novel Biomarker for Colorectal Cancer with Prognostic Relevance
by Eva Parisi, Ivan Hidalgo, Robert Montal, Ona Pallisé, Jordi Tarragona, Anabel Sorolla, Anna Novell, Kyra Campbell, Maria Alba Sorolla, Andreu Casali and Antonieta Salud
Int. J. Mol. Sci. 2023, 24(13), 10889; https://doi.org/10.3390/ijms241310889 - 30 Jun 2023
Cited by 1 | Viewed by 2632
Abstract
Metastasis is the leading cause of colorectal cancer (CRC)-related deaths. Therefore, the identification of accurate biomarkers predictive of metastasis is needed to better stratify high-risk patients to provide preferred management and reduce mortality. In this study, we identified 13 new genes that modified [...] Read more.
Metastasis is the leading cause of colorectal cancer (CRC)-related deaths. Therefore, the identification of accurate biomarkers predictive of metastasis is needed to better stratify high-risk patients to provide preferred management and reduce mortality. In this study, we identified 13 new genes that modified circulating tumor cell numbers using a genome-wide genetic screen in a whole animal CRC model. Candidate genes were subsequently evaluated at the gene expression level in both an internal human CRC cohort of 153 patients and an independent cohort from the TCGA including 592 patients. Interestingly, the expression of one candidate, PLA2G12A, significantly correlated with both the time to recurrence and overall survival in our CRC cohort, with its low expression being an indicator of a poor clinical outcome. By examining the TCGA cohort, we also found that low expression of PLA2G12A was significantly enriched in epithelial–mesenchymal transition signatures. Finally, the candidate functionality was validated in vitro using three different colon cancer cell lines, revealing that PLA2G12A deficiency increases cell proliferation, migration, and invasion. Overall, our study identifies PLA2G12A as a prognostic biomarker of early-stage CRC, providing evidence that its deficiency promotes tumor growth and dissemination. Full article
(This article belongs to the Special Issue Molecular Advances in Colorectal Cancer)
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19 pages, 3564 KiB  
Article
Combinatorial Network of Transcriptional and miRNA Regulation in Colorectal Cancer
by Rupesh Kumar, Maged Mostafa Mahmoud, Hanaa M. Tashkandi, Shafiul Haque, Steve Harakeh, Kalaiarasan Ponnusamy and Shazia Haider
Int. J. Mol. Sci. 2023, 24(6), 5356; https://doi.org/10.3390/ijms24065356 - 10 Mar 2023
Cited by 1 | Viewed by 2355
Abstract
Colorectal cancer is one of the leading causes of cancer-associated mortality across the worldwide. One of the major challenges in colorectal cancer is the understanding of the regulatory mechanisms of biological molecules. In this study, we aimed to identify novel key molecules in [...] Read more.
Colorectal cancer is one of the leading causes of cancer-associated mortality across the worldwide. One of the major challenges in colorectal cancer is the understanding of the regulatory mechanisms of biological molecules. In this study, we aimed to identify novel key molecules in colorectal cancer by using a computational systems biology approach. We constructed the colorectal protein–protein interaction network which followed hierarchical scale-free nature. We identified TP53, CTNBB1, AKT1, EGFR, HRAS, JUN, RHOA, and EGF as bottleneck-hubs. The HRAS showed the largest interacting strength with functional subnetworks, having strong correlation with protein phosphorylation, kinase activity, signal transduction, and apoptotic processes. Furthermore, we constructed the bottleneck-hubs’ regulatory networks with their transcriptional (transcription factor) and post-transcriptional (miRNAs) regulators, which exhibited the important key regulators. We observed miR-429, miR-622, and miR-133b and transcription factors (EZH2, HDAC1, HDAC4, AR, NFKB1, and KLF4) regulates four bottleneck-hubs (TP53, JUN, AKT1 and EGFR) at the motif level. In future, biochemical investigation of the observed key regulators could provide further understanding about their role in the pathophysiology of colorectal cancer. Full article
(This article belongs to the Special Issue Molecular Advances in Colorectal Cancer)
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13 pages, 2022 KiB  
Article
PARP-1 Expression Influences Cancer Stem Cell Phenotype in Colorectal Cancer Depending on p53
by Jose D. Puentes-Pardo, Sara Moreno-SanJuan, Jorge Casado, Julia Escudero-Feliu, David López-Pérez, Paula Sánchez-Uceta, Paula González-Novoa, Julio Gálvez, Ángel Carazo and Josefa León
Int. J. Mol. Sci. 2023, 24(5), 4787; https://doi.org/10.3390/ijms24054787 - 1 Mar 2023
Cited by 7 | Viewed by 2557
Abstract
Poly(ADP-ribose) polymerase-1 (PARP-1) is a protein involved in multiple physiological processes. Elevated PARP-1 expression has been found in several tumours, being associated with stemness and tumorigenesis. In colorectal cancer (CRC), some controversy among studies has been described. In this study, we analysed the [...] Read more.
Poly(ADP-ribose) polymerase-1 (PARP-1) is a protein involved in multiple physiological processes. Elevated PARP-1 expression has been found in several tumours, being associated with stemness and tumorigenesis. In colorectal cancer (CRC), some controversy among studies has been described. In this study, we analysed the expression of PARP-1 and cancer stem cell (CSC) markers in CRC patients with different p53 status. In addition, we used an in vitro model to evaluate the influence of PARP-1 in CSC phenotype regarding p53. In CRC patients, PARP-1 expression correlated with the differentiation grade, but this association was only maintained for tumours harbouring wild-type p53. Additionally, in those tumours, PARP-1 and CSC markers were positively correlated. In mutated p53 tumours, no associations were found, but PARP-1 was an independent factor for survival. According to our in vitro model, PARP-1 regulates CSC phenotype depending on p53 status. PARP-1 overexpression in a wild type p53 context increases CSC markers and sphere forming ability. By contrast, those features were reduced in mutated p53 cells. These results could implicate that patients with elevated PARP-1 expression and wild type p53 could benefit from PARP-1 inhibition therapies, meanwhile it could have adverse effects for those carrying mutated p53 tumours. Full article
(This article belongs to the Special Issue Molecular Advances in Colorectal Cancer)
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17 pages, 3187 KiB  
Article
Asparagine and Glutamine Deprivation Alters Ionizing Radiation Response, Migration and Adhesion of a p53null Colorectal Cancer Cell Line
by Isabella Guardamagna, Ombretta Iaria, Leonardo Lonati, Alice Mentana, Andrea Previtali, Virginia Uggè, Giovanni Battista Ivaldi, Marco Liotta, Paola Tabarelli de Fatis, Claudia Scotti, Greta Pessino, Maristella Maggi and Giorgio Baiocco
Int. J. Mol. Sci. 2023, 24(3), 2983; https://doi.org/10.3390/ijms24032983 - 3 Feb 2023
Cited by 3 | Viewed by 2736
Abstract
Colorectal cancer (CRC) is the most prominent form of colon cancer for both incidence (38.7 per 100,000 people) and mortality (13.9 per 100,000 people). CRC’s poor response to standard therapies is linked to its high heterogeneity and complex genetic background. Dysregulation or depletion [...] Read more.
Colorectal cancer (CRC) is the most prominent form of colon cancer for both incidence (38.7 per 100,000 people) and mortality (13.9 per 100,000 people). CRC’s poor response to standard therapies is linked to its high heterogeneity and complex genetic background. Dysregulation or depletion of the tumor suppressor p53 is involved in CRC transformation and its capability to escape therapy, with p53null cancer subtypes known, in fact, to have a poor prognosis. In such a context, new therapeutic approaches aimed at reducing CRC proliferation must be investigated. In clinical practice, CRC chemotherapy is often combined with radiation therapy with the aim of blocking the expansion of the tumor mass or removing residual cancer cells, though contemporary targeting of amino acid metabolism has not yet been explored. In the present study, we used the p53null Caco-2 model cell line to evaluate the effect of a possible combination of radiation and L-Asparaginase (L-ASNase), a protein drug that blocks cancer proliferation by impairing asparagine and glutamine extracellular supply. When L-ASNase was administered immediately after IR, we observed a reduced proliferative capability, a delay in DNA-damage response and a reduced capability to adhere and migrate. Our data suggest that a correctly timed combination of X-rays and L-ASNase treatment could represent an advantage in CRC therapy. Full article
(This article belongs to the Special Issue Molecular Advances in Colorectal Cancer)
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19 pages, 6209 KiB  
Article
Inhibition of GABAAR or Application of Lactobacillus casei Zhang Alleviates Ulcerative Colitis in Mice: GABAAR as a Potential Target for Intestinal Epithelial Renewal and Repair
by Qiuzhen Wang, Ziteng Deng, Jing Lan, Dan Li, Kai Fan, Jianyu Chang and Yunfei Ma
Int. J. Mol. Sci. 2022, 23(19), 11210; https://doi.org/10.3390/ijms231911210 - 23 Sep 2022
Cited by 8 | Viewed by 2416
Abstract
Emerging evidence indicates that the gamma−aminobutyric acid type A receptor (GABAAR) and Lactobacillus casei Zhang regulate colitis in a variety of ways, such as by participating in host immune and inflammatory responses, altering the gut microbiota, and influencing intestinal barrier function. [...] Read more.
Emerging evidence indicates that the gamma−aminobutyric acid type A receptor (GABAAR) and Lactobacillus casei Zhang regulate colitis in a variety of ways, such as by participating in host immune and inflammatory responses, altering the gut microbiota, and influencing intestinal barrier function. However, not much is known about the mechanisms by which GABAAR and L. casei affect colon epithelial cell renewal and the interaction between GABAAR and L. casei during this process. To elucidate this, we established a dextran sulfate sodium (DSS)−induced model and measured the mouse body weights, colon length, the disease activity index (DAI), and histological scores. Our results indicated that inhibition of GABAAR alleviated the DSS−induced colitis symptoms, resulting in less weight loss and more intact colon tissue. Moreover, treatment with bicuculline (Bic, a GABAAR inhibitor) increased the levels of PCNA, β−catenin, and TCF4 in mice with colitis. Interestingly, open field test performances showed that inhibition of GABAAR also attenuated colitis−related anxiety−like behavior. By 16S RNA gene sequencing analysis, we showed that inhibition of GABAAR partially reversed the gut dysbacteriosis of DSS−induced mice and increased the abundance of beneficial bacteria. Additionally, L. casei Zhang supplementation inhibited the expression of GABAAR in mice with colitis, promoted the proliferation and renewal of colon epithelial cells, and alleviated anxiety−like behavior and intestinal microflora disorder in mice. Thus, GABAAR plays a key role in the beneficial effects of L. casei on DSS−induced colitis in mice. Full article
(This article belongs to the Special Issue Molecular Advances in Colorectal Cancer)
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