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Molecular Mechanisms of Inhibition of Colorectal Cancer
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Molecular Mechanisms of Inhibition of Colorectal Cancer

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: closed (31 August 2024) | Viewed by 7435

Special Issue Editor

Dr. Jennifer Haynes

E-Mail Website
Guest Editor
Department of Clinical and Translational Sciences, Marshall University School of Medicine, Huntington, WV, USA
Interests: colorectal cancer; cancer cell biology; cancer stem cells; 3D organoids; intestinal epithelial cells; nutrient transport; obesity

Special Issue Information

Dear Colleagues,

Colorectal cancer (CRC) is the second leading cause of cancer-related death worldwide, and its incidence rates are rising, especially among younger adults (<50 years). Late-stage CRC in particular has a high risk of recurrence, despite surgery and adjuvant chemotherapy or chemoradiotherapy. Thus, the search for new treatment strategies to inhibit CRC is extremely relevant to improving the life expectancy of CRC patients.

In recent years, investigations into the biology of CRC have led to a rapid increase in our understanding of the molecular and epigenetic mechanisms that regulate CRC cell proliferation, survival, and stemness, as well as the contribution of the tumor microenvironment to CRC growth and metastasis. This knowledge has continually led to advancements in therapeutic approaches to inhibit CRC, including molecular-targeted drugs and immunotherapy, which are in turn facilitating a trend toward precision medicine for the future of CRC treatment.

This Special Issue of IJMS, “Molecular Mechanisms of Inhibition of Colorectal Cancer”, is pleased to invite you to contribute original research articles describing basic or translational studies on topics including, but not limited to, the molecular mechanisms involved in inhibiting the proliferation, angiogenesis, invasion, or metastasis of CRC cells. Literature reviews summarizing current and emerging therapeutic approaches being used to inhibit CRC and the molecular pathways and mechanisms involved are also welcome. A deeper understanding of the molecular mechanisms that inhibit CRC growth and metastasis will lead to the development of novel molecular-targeted therapeutics and advanced combination therapies that are more effective, with fewer side effects and less resistant.

Dr. Jennifer Haynes
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

  • colorectal cancer (CRC)
  • molecular mechanisms
  • mechanisms of inhibition
  • cancer therapies
  • chemotherapy
  • immunotherapy
  • small molecule inhibitors
  • molecular therapeutic targets
  • signaling pathways
  • proliferation
  • angiogenesis
  • invasion
  • metastasis
  • cancer stem cells
  • tumor microenvironment

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Published Papers (4 papers)

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Research

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15 pages, 6006 KiB  
Article
NRXN1 as a Prognostic Biomarker: Linking Copy Number Variation to EMT and Survival in Colon Cancer
by Hyun Jin Bang, Hyun-Jeong Shim, Mi-Ra Park, Sumin Yoon, Kyung Hyun Yoo, Young-Kook Kim, Hyunju Lee, Jeong-Seok Nam, Jun-Eul Hwang, Woo-Kyun Bae, Ik-Joo Chung, Eun-Gene Sun and Sang-Hee Cho
Int. J. Mol. Sci. 2024, 25(21), 11423; https://doi.org/10.3390/ijms252111423 - 24 Oct 2024
Viewed by 1249
Abstract
The role of biomarkers in cancer treatment varies significantly depending on the cancer stage. Thus, in clinical practice, tailoring biomarkers to meet the specific needs and challenges of each cancer stage can increase the precision of treatment. Because they reflect underlying genetic alterations [...] Read more.
The role of biomarkers in cancer treatment varies significantly depending on the cancer stage. Thus, in clinical practice, tailoring biomarkers to meet the specific needs and challenges of each cancer stage can increase the precision of treatment. Because they reflect underlying genetic alterations that influence cancer progression, copy number variation (CNV) biomarkers can play crucial prognostic roles. In our previous study, we identified potential survival-related genes for colorectal cancer (CRC) by analyzing CNV and gene expression data using a machine-learning approach. To further investigate the biological function of NRXN1, we assessed the use of RNA sequencing, phosphokinase assays, real-time quantitative PCR, and Western blot analysis. We found that NRXN1 copy number deletion was significantly associated with poor overall survival (OS) and recurrence-free survival (RFS), even in patients who received adjuvant chemotherapy. Compared with its expression in normal tissues, NRXN1 expression was lower in tumors, suggesting its potential role as a tumor suppressor. NRXN1 knockdown enhanced CRC cell viability and invasion, and transcriptome analysis indicated that the increased invasion was caused by GSK3β-mediated epithelial–mesenchymal transition. These findings highlight NRXN1 copy number deletion as a novel biomarker for predicting recurrence and survival in patients with resected colon cancer. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Inhibition of Colorectal Cancer)
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14 pages, 3472 KiB  
Article
Overexpression of Fatty Acid Synthase Upregulates Glutamine–Fructose-6-Phosphate Transaminase 1 and O-Linked N-Acetylglucosamine Transferase to Increase O-GlcNAc Protein Glycosylation and Promote Colorectal Cancer Growth
by James Drury, Mariah E. Geisen, Josiane Weber Tessmann, Piotr G. Rychahou, Courtney O. Kelson, Daheng He, Chi Wang, B. Mark Evers and Yekaterina Y. Zaytseva
Int. J. Mol. Sci. 2024, 25(9), 4883; https://doi.org/10.3390/ijms25094883 - 30 Apr 2024
Cited by 4 | Viewed by 2071
Abstract
Fatty acid synthesis has been extensively investigated as a therapeutic target in cancers, including colorectal cancer (CRC). Fatty acid synthase (FASN), a key enzyme of de novo lipid synthesis, is significantly upregulated in CRC, and therapeutic approaches of targeting this enzyme are currently [...] Read more.
Fatty acid synthesis has been extensively investigated as a therapeutic target in cancers, including colorectal cancer (CRC). Fatty acid synthase (FASN), a key enzyme of de novo lipid synthesis, is significantly upregulated in CRC, and therapeutic approaches of targeting this enzyme are currently being tested in multiple clinical trials. However, the mechanisms behind the pro-oncogenic action of FASN are still not completely understood. Here, for the first time, we show that overexpression of FASN increases the expression of glutamine–fructose-6-phosphate transaminase 1 (GFPT1) and O-linked N-acetylglucosamine transferase (OGT), enzymes involved in hexosamine metabolism, and the level of O-GlcNAcylation in vitro and in vivo. Consistently, expression of FASN significantly correlates with expression of GFPT1 and OGT in human CRC tissues. shRNA-mediated downregulation of GFPT1 and OGT inhibits cellular proliferation and the level of protein O-GlcNAcylation in vitro, and knockdown of GFPT1 leads to a significant decrease in tumor growth and metastasis in vivo. Pharmacological inhibition of GFPT1 and OGT leads to significant inhibition of cellular proliferation and colony formation in CRC cells. In summary, our results show that overexpression of FASN increases the expression of GFPT1 and OGT as well as the level of protein O-GlcNAcylation to promote progression of CRC; targeting the hexosamine biosynthesis pathway could be a therapeutic approach for this disease. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Inhibition of Colorectal Cancer)
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18 pages, 4241 KiB  
Article
Mitotic Spindle Positioning (MISP) Facilitates Colorectal Cancer Progression by Forming a Complex with Opa Interacting Protein 5 (OIP5) and Activating the JAK2-STAT3 Signaling Pathway
by Koki Hiura, Masaki Watanabe, Naoki Hirose, Kenta Nakano, Tadashi Okamura, Hayato Sasaki and Nobuya Sasaki
Int. J. Mol. Sci. 2024, 25(5), 3061; https://doi.org/10.3390/ijms25053061 - 6 Mar 2024
Cited by 2 | Viewed by 1765
Abstract
Patients with inflammatory bowel disease (IBD) who experience long-term chronic inflammation of the colon are at an increased risk of developing colorectal cancer (CRC). Mitotic spindle positioning (MISP), an actin-binding protein, plays a role in mitosis and spindle positioning. MISP is found on [...] Read more.
Patients with inflammatory bowel disease (IBD) who experience long-term chronic inflammation of the colon are at an increased risk of developing colorectal cancer (CRC). Mitotic spindle positioning (MISP), an actin-binding protein, plays a role in mitosis and spindle positioning. MISP is found on the apical membrane of the intestinal mucosa and helps stabilize and elongate microvilli, offering protection against colitis. This study explored the role of MISP in colorectal tumorigenesis using a database, human CRC cells, and a mouse model for colitis-induced colorectal tumors triggered by azoxymethane (AOM)/dextran sodium sulfate (DSS) treatment. We found that MISP was highly expressed in colon cancer patient tissues and that reduced MISP expression inhibited cell proliferation. Notably, MISP-deficient mice showed reduced colon tumor formation in the AOM/DSS-induced colitis model. Furthermore, MISP was found to form a complex with Opa interacting protein 5 (OIP5) in the cytoplasm, influencing the expression of OIP5 in a unidirectional manner. We also observed that MISP increased the levels of phosphorylated STAT3 in the JAK2-STAT3 signaling pathway, which is linked to tumorigenesis. These findings indicate that MISP could be a risk factor for CRC, and targeting MISP might provide insights into the mechanisms of colitis-induced colorectal tumorigenesis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Inhibition of Colorectal Cancer)
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Review

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20 pages, 1435 KiB  
Review
Redefining Therapeutic Approaches in Colorectal Cancer: Targeting Molecular Pathways and Overcoming Resistance
by Simona Gabriela Duta-Ion, Ioana Ruxandra Juganaru, Iulian Andrei Hotinceanu, Andra Dan, Livia Malina Burtavel, Madalin Codrut Coman, Ina Ofelia Focsa, Andra Giorgiana Zaruha, Patricia Christina Codreanu, Laurentiu Camil Bohiltea and Viorica Elena Radoi
Int. J. Mol. Sci. 2024, 25(23), 12507; https://doi.org/10.3390/ijms252312507 - 21 Nov 2024
Viewed by 1548
Abstract
Colorectal cancer (CRC) arises through a combination of genetic and epigenetic alterations that affect key pathways involved in tumor growth and progression. This review examines the major molecular pathways driving CRC, including Chromosomal Instability (CIN), Microsatellite Instability (MSI), and the CpG Island Methylator [...] Read more.
Colorectal cancer (CRC) arises through a combination of genetic and epigenetic alterations that affect key pathways involved in tumor growth and progression. This review examines the major molecular pathways driving CRC, including Chromosomal Instability (CIN), Microsatellite Instability (MSI), and the CpG Island Methylator Phenotype (CIMP). Key mutations in genes such as APC, KRAS, NRAS, BRAF, and TP53 activate signaling pathways like Wnt, EGFR, and PI3K/AKT, contributing to tumorigenesis and influencing responses to targeted therapies. Resistance mechanisms, including mutations that bypass drug action, remain challenging in CRC treatment. This review highlights the role of molecular profiling in guiding the use of targeted therapies such as tyrosine kinase inhibitors and immune checkpoint inhibitors. Novel combination treatments are also discussed as strategies to improve outcomes and overcome resistance. Understanding these molecular mechanisms is critical to advancing personalized treatment approaches in CRC and improving patient prognosis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Inhibition of Colorectal Cancer)
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