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Molecular Mechanisms and Therapeutic Strategies of Colorectal Cancer
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Molecular Mechanisms and Therapeutic Strategies 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: 20 February 2026 | Viewed by 1891

Special Issue Editor

Dr. Daniel Gabriel Pons

E-Mail Website
Guest Editor
1. Multidisciplinar Group in Traslational Oncology (GMOT), Balearic Islands University (UIB), 07122 Palma, Spain
2. Balearic Islands Health Research Institute (IdISBa), 07010 Palma, Spain
Interests: oxidative stress; estrogen; phytoestrogens; cancer cells; personalized treatment
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Colorectal cancer (CRC) remains one of the most prevalent and lethal malignancies worldwide, necessitating advancements in understanding its underlying mechanisms and therapeutic strategies. This Special Issue, entitled “Molecular Mechanisms and Therapeutic Strategies of Colorectal Cancer”, aims to gather innovative research on the molecular and cellular processes driving the development, progression, and resistance of CRC to treatment. This Special Issue will particularly focus on novel biomarkers for early detection, the role of the tumor microenvironment, advancements in immunotherapy, and innovative therapeutic approaches that target signaling pathways. Contributions that explore precision medicine strategies, the potential application of phytochemicals or bioactive compounds as adjuvant therapies, and the use of extracellular vesicles for intercellular communication are particularly welcome. By integrating multidisciplinary perspectives, this Special Issue seeks to highlight breakthroughs that can translate into improved clinical outcomes for CRC patients.

Dr. Daniel Gabriel Pons
Guest Editor

Manuscript Submission Information

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Keywords

  • colorectal cancer
  • tumor microenvironment
  • biomarkers
  • intercellular communication
  • therapeutic strategies

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Published Papers (2 papers)

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18 pages, 6015 KB  
Article
Biomarker Identification via Spatial Transcriptomics Profiling of Colorectal Cancer and Colorectal Cancer with Liver Metastasis Stem Cells
by Minho Lee, Seoin Han, Hak Chun Kim, Yujun Jung, Jeong-An Gim, Chang-Jin Kim and Dongjun Jeong
Int. J. Mol. Sci. 2025, 26(22), 11045; https://doi.org/10.3390/ijms262211045 - 14 Nov 2025
Viewed by 605
Abstract
Colorectal cancer (CRC) demonstrates favorable clinical outcomes when diagnosed at an early stage; however, the prognosis declines substantially following recurrence or distant metastasis. Increasing evidence indicates that cancer stem cells (CSCs) are pivotal contributors to tumor recurrence, metastatic dissemination, and therapeutic resistance. The [...] Read more.
Colorectal cancer (CRC) demonstrates favorable clinical outcomes when diagnosed at an early stage; however, the prognosis declines substantially following recurrence or distant metastasis. Increasing evidence indicates that cancer stem cells (CSCs) are pivotal contributors to tumor recurrence, metastatic dissemination, and therapeutic resistance. The present study aimed to identify CSC-associated biomarkers through spatial transcriptomic profiling of normal colonic mucosa, primary CRC, and liver metastatic tissues, and to evaluate their functional relevance in CRC progression. Spatial transcriptomic analysis revealed that CCN2 was preferentially enriched within CSC clusters of primary CRC tissues, whereas APOC2 was predominantly upregulated in liver-metastatic CSCs. Functional validation of CCN2 was performed by establishing CCN2-knockout HCT116 cell lines using the CRISPR-Cas9 system. Loss of CCN2 expression markedly attenuated cell proliferation, migration, invasion, and oxaliplatin resistance compared with control cells. Furthermore, immunohistochemical analysis of tissue microarrays demonstrated a significant positive correlation between CCN2 expression and CSC markers SOX2 and Nestin. Collectively, these findings suggest that CCN2 functions as a central regulator of stemness and malignant potential in CRC and may represent a promising therapeutic target to prevent recurrence and metastasis. Additional mechanistic studies are warranted to further elucidate the molecular pathways of CCN2 and to validate the role of APOC2 in liver-metastatic CRC stem cells. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Strategies of Colorectal Cancer)
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22 pages, 4133 KB  
Article
Multiomics Signature Reveals Network Regulatory Mechanisms in a CRC Continuum
by Juan Carlos Higareda-Almaraz, Francesco Mattia Mancuso, Pol Canal-Noguer, Kristi Kruusmaa and Arianna Bertossi
Int. J. Mol. Sci. 2025, 26(15), 7077; https://doi.org/10.3390/ijms26157077 - 23 Jul 2025
Viewed by 903
Abstract
Sporadic colorectal cancer (CRC), the third leading cause of cancer-related death globally, arises through a continuum from normal tissue to adenomas, progressing from low-grade (LGD) to high-grade dysplasia (HGD); yet, the early epigenetic drivers of this transition remain unclear. To investigate these events, [...] Read more.
Sporadic colorectal cancer (CRC), the third leading cause of cancer-related death globally, arises through a continuum from normal tissue to adenomas, progressing from low-grade (LGD) to high-grade dysplasia (HGD); yet, the early epigenetic drivers of this transition remain unclear. To investigate these events, we profiled LGD and HGD adenomas using EM-seq, and identified a consensus differential methylation signature (DMS) of 626 regions through two independent bioinformatics pipelines. This signature effectively distinguished LGD from HGD in both tissue and plasma-derived cell-free DNA (cfDNA), highlighting specific methylation patterns. Functional annotation indicated enrichment for regulatory elements associated with transcription factor activity and cell signaling. Applying the DMS to the TCGA CRC dataset revealed three tumor subtypes with increasing hypermethylation and one normal cluster. The most hypermethylated subtype exhibited poor survival, high mutation burden, and disrupted transcriptional networks. While overlapping with classical CpG Island Methylator Phenotype (CIMP) categories, the DMS captured a broader spectrum of methylation alterations. These findings suggest that the DMS captures functionally relevant, antecedent epigenetic alterations in CRC progression, enabling the robust stratification of dysplasia severity and tumor subtypes. This signature holds promise for enhancing preclinical detection and molecular classification, and warrants further evaluation in larger prospective cohorts. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Strategies of Colorectal Cancer)
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