Advances in Molecular Mechanisms of Gastrointestinal Tumors (2nd Edition)

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 25 November 2025 | Viewed by 1283

Special Issue Editor


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Guest Editor
Division of Risk Assessment, Center for Biological Safety and Research, National Institute of Health Sciences, Kawasaki 210-9501, Japan
Interests: molecular network in diseases; signaling pathway in cancer; molecular mechanism in cancer therapy; therapeutic response in cancer
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Special Issue Information

Dear Colleagues,

This Special Issue is the second edition of the Special Issue titled “Advances in Molecular Mechanisms of Gastrointestinal Tumors” (https://www.mdpi.com/journal/cancers/special_issues/molecular_gastrointestinal).

We are pleased to invite you to contribute to this Special Issue, titled “Advances in Molecular Mechanisms of Gastrointestinal Tumors (2nd edition)”, of Cancers. Gastrointestinal cancer is one of the most common malignancies worldwide. The molecular mechanisms of gastrointestinal cancer, and particularly several subtypes that are resistant to treatment, have not been fully elucidated.

This Special Issue aims to reveal the mechanisms of gastrointestinal tumors, where molecular pathway networks are involved. The molecular mechanism of gastrointestinal tumors is the main scope of this Special Issue.

For this Special Issue, original research articles and reviews are welcome. Research areas may include, but are not limited to, the following:

Molecular mechanisms, gastrointestinal tumors, gastric cancer, colon cancer, rectal cancer, colorectal cancer, esophageal cancer, cancer stem cell, tumor microenvironment, molecular pathways, molecular networks, pathway networks.

We look forward to receiving your contributions.

Dr. Shihori Tanabe
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 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. Cancers 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 2900 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

  • molecular mechanism
  • gastrointestinal tumor
  • gastric cancer
  • colorectal cancer
  • esophageal cancer
  • tumor microenvironment
  • molecular network
  • molecular pathway
  • pathway network
  • signal transduction

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Published Papers (2 papers)

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17 pages, 8548 KiB  
Article
miR-195-5p Suppresses KRT80 Expression Inducing Cell Cycle Arrest in Colon Cancer
by Emanuele Piccinno, Viviana Scalavino, Nicoletta Labarile, Giusy Bianco, Raffaele Armentano, Gianluigi Giannelli and Grazia Serino
Cancers 2025, 17(13), 2183; https://doi.org/10.3390/cancers17132183 - 28 Jun 2025
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Abstract
Background/Objectives: Keratins form a crucial component of the epithelial cytoskeleton, playing an essential role in maintaining tissue architecture and coordinating key cellular functions. KRT80 is a type II keratin that has emerged as an oncogenic driver in several malignancies, yet its involvement in [...] Read more.
Background/Objectives: Keratins form a crucial component of the epithelial cytoskeleton, playing an essential role in maintaining tissue architecture and coordinating key cellular functions. KRT80 is a type II keratin that has emerged as an oncogenic driver in several malignancies, yet its involvement in colorectal cancer (CRC) remains unclear. Here, we investigated the molecular interaction between miR-195-5p, KRT80 expression, and CRC growth. Methods: Potential miR-195-5p binding sites in the KRT80 3′-UTR were identified through the use of integrated bioinformatic analyses, while publicly available datasets confirmed a significant overexpression of KRT80 in CRC tissues compared to normal mucosa. This finding was further validated through the use of mRNA and protein analysis in paired tumor and adjacent normal samples from CRC patients. Results: Functional assays involving CRC cell lines showed that transfection with miR-195-5p mimics led to a significant downregulation of KRT80 expression, reflecting the effects of direct KRT80 silencing by siRNA. Both molecular approaches induced G1-phase cell cycle arrest, concomitantly with reductions in G2/M populations. Furthermore, the in vivo delivery of miR-195-5p mimics in a mouse model of colitis-associated CRC resulted in a significant reduction in Krt80 expression in the colon. Conclusions: Collectively, our results reveal that miR-195-5p negatively regulates KRT80 expression, contributing to its tumor-suppressive activity in colorectal cancer and highlighting a molecular mechanism with potential therapeutic relevance. Full article
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21 pages, 1343 KiB  
Review
The Evolving Landscape of GEP-NENs in the Era of Precision Oncology: Molecular Insights into Tumor Heterogeneity
by Sunanda Biswas Mukherjee, Rachyl M. Shanker, James P. Madigan and Samira M. Sadowski
Cancers 2025, 17(13), 2080; https://doi.org/10.3390/cancers17132080 - 21 Jun 2025
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Abstract
Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) are a varied group of tumors that originate from neuroendocrine cells found throughout the gastrointestinal tract. These tumors encompass a broad spectrum of biological behaviors, ranging from slow-growing, well-differentiated neuroendocrine tumors (GEP-NETs) to aggressive and poorly differentiated neuroendocrine carcinomas [...] Read more.
Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) are a varied group of tumors that originate from neuroendocrine cells found throughout the gastrointestinal tract. These tumors encompass a broad spectrum of biological behaviors, ranging from slow-growing, well-differentiated neuroendocrine tumors (GEP-NETs) to aggressive and poorly differentiated neuroendocrine carcinomas (GEP-NECs), complicating their accurate classification and effective treatment. While advances in molecular research have refined our understanding of these tumors, their complexity, unpredictable progression, and differential response to therapies remain major clinical hurdles. A significant clinical challenge is the accurate grading and diagnosis of GEP-NENs, which is traditionally reliant on subjective methods. However, innovative technologies, such as artificial intelligence-based diagnostics, multi-omics approaches, and precision oncology, are now offering solutions for more precise and reliable classification. Meanwhile, emerging therapies aiming to activate the immune response or modify the tumor environment present promising avenues for improved outcomes. Realizing the full potential of these advances will require a thoughtful integration of molecular insights with standardized diagnostic practices and evolving therapeutic strategies, ensuring that progress in research meaningfully informs and enhances patient care across diverse clinical settings. This review discusses new advancements and explores future directions toward personalized and effective treatments for GEP-NENs. Full article
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