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Molecular Targets in Gastrointestinal Diseases

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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 (20 January 2026) | Viewed by 9395

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Prof. Dr. Changwon Yang

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Guest Editor

Department of Science Education, Ewha Womans University, Seoul 03760, Republic of Korea
Interests: oncology; gestational disease; reproduction; drug resistance; metabolic disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, entitled “Molecular Targets in Gastrointestinal Diseases”, invites researchers to explore and submit their latest findings on the molecular underpinnings of gastrointestinal (GI) diseases. This Special Issue aims to highlight the critical molecular mechanisms and targets that drive the pathology of a wide range of GI conditions, including inflammatory diseases, carcinomas, metabolic disorders, and functional gastrointestinal disorders.

Understanding the molecular targets in GI diseases is crucial for the development of innovative therapeutic strategies. This includes the identification of key signaling pathways, genetic mutations, epigenetic modifications, and protein interactions that contribute to disease onset and progression. By elucidating these molecular mechanisms, researchers will be able to pave the way for targeted therapies that offer improved efficacy and reduced side effects compared to traditional treatments.

The scope of this Special Issue encompasses, but is not limited to, the following topics:

Novel molecular targets in GI cancers such as colorectal, gastric, and pancreatic cancer;
Insights into the molecular basis of inflammatory bowel diseases (IBDs) like Crohn’s disease and ulcerative colitis;
Molecular pathways involved in gastroesophageal reflux disease (GERD) and irritable bowel syndrome (IBS);
The role of microbiota and its metabolites in modulating GI disease states.

This Special Issue seeks to foster a deeper understanding of the molecular landscape of GI diseases and inspire novel approaches for diagnosis, treatment, and prevention. Join us in contributing to this pivotal collection, aiming to transform the landscape of gastrointestinal disease management through molecular insights.

Prof. Dr. Changwon Yang
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

molecular pathways
gastrointestinal cancers
inflammatory bowel disease
targeted therapies
microbiota
gene editing

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Published Papers (5 papers)

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Research

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16 pages, 4259 KB

Open AccessArticle

Panobinostat Potentiates the Antitumor Efficacy of 5-Fluorouracil in Gastric Cancer by Suppressing Thymidylate Synthase Expression

by Sooyeon Park, Nayeon Kim and Changwon Yang

Int. J. Mol. Sci. 2026, 27(3), 1516; https://doi.org/10.3390/ijms27031516 - 3 Feb 2026

Viewed by 658

Abstract

Resistance to 5-fluorouracil (5-FU), a cornerstone chemotherapy for gastric cancer (GC), is a major clinical obstacle, often driven by the upregulation of its target enzyme, thymidylate synthase (TS). In this study, we investigated the potential of the pan-histone deacetylase inhibitor (HDACi) panobinostat to synergize with 5-FU. In GC cell lines, panobinostat treatment alone suppressed cell viability, clonogenicity, and migration, and this was associated with the induction of G1-phase cell cycle arrest and mitochondria-mediated apoptosis. Crucially, Panobinostat acted synergistically with 5-FU, leading to enhanced cytotoxicity. Mechanistically, 5-FU treatment alone induced a compensatory upregulation of TS protein, a known resistance mechanism. Panobinostat not only suppressed basal TS expression but, more importantly, abrogated this 5-FU-induced upregulation. Furthermore, panobinostat downregulated a network of oncogenes and cell cycle regulators, including c-Myc and key cyclins. These findings indicate that panobinostat can enhance 5-FU cytotoxicity by targeting TS expression and reprogramming oncogenic transcriptional networks, supporting its potential as a complementary strategy for overcoming fluoropyrimidine resistance in GC therapy. Full article

(This article belongs to the Special Issue Molecular Targets in Gastrointestinal Diseases)

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22 pages, 4163 KB

Open AccessArticle

Comparative Analysis of Mucosa-Associated and Luminal Gut Microbiota in Pediatric Ulcerative Colitis

by Takeo Kondo, Sonoko Kondo, Haruyuki Nakayama-Imaohji, Ayano Tada, Nafisa Tabassum, Emmanuel Munyeshyaka, Kosuke Koyano, Shinji Nakamura, Takashi Kusaka and Tomomi Kuwahara

Int. J. Mol. Sci. 2025, 26(21), 10775; https://doi.org/10.3390/ijms262110775 - 5 Nov 2025

Cited by 2 | Viewed by 1692

Abstract

Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease, are chronic disorders relating to gut microbiota dysbiosis. Despite severe pancolitis being more prevalent in pediatric UC than in adults, alterations in the colon mucosa-associated microbiota (MAM) and their association with disease severity remain to be elucidated. The present study aimed to compare the gut microbiota in colon lavage fluids (CLFs) and fecal samples from 19 pediatric UC and 19 non-IBD patients. The community structure of MAM inferred by 16S metagenomic analysis was similar throughout the colon regardless of disease type. Bacterial compositions between MAM and feces were significantly different in non-IBD, while no difference was observed in pediatric UC, indicating a compromised mucous layer that could not sufficiently separate the MAM and luminal microbiota in UC. In pediatric UC, homogenous distribution of MAM was gradually disordered with increases in disease activity or mucosal inflammation, and bacterial groups of upper digestive tract or environmental origin were more abundant in MAM. Monitoring key bacterial markers in MAM, which include Lactobacillus and Enterococcus or Faecalibacterium and Blautia as increased or reduced members in pediatric UC, respectively, might be useful for evaluation of patient prognosis. Full article

(This article belongs to the Special Issue Molecular Targets in Gastrointestinal Diseases)

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Review

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17 pages, 666 KB

Open AccessReview

Microbiome Signatures in Advanced Gastric Cancer: Emerging Biomarkers for Risk Stratification, Therapy Guidance, and Prognostic Insight

by Kyung-il John Kim, Hannah Zhong, Derek Tai, Pranati Shah, Daniel Park, Vitor Goes, Jianan Li, Claire Jung, Lucas Kim, Sofia Guzman, Gagandeep Brar and Dani Castillo

Int. J. Mol. Sci. 2026, 27(3), 1452; https://doi.org/10.3390/ijms27031452 - 31 Jan 2026

Cited by 2 | Viewed by 1257

Abstract

Gastric cancer (GC), often diagnosed at advanced or metastatic stages, remains a significant clinical challenge requiring novel biomarkers for early detection, risk stratification, and effective, personalized treatment optimization. Emerging evidence underscores a strong association between gut microbiome dysbiosis and GC initiation, progression, and therapeutic outcomes. This review explores the potential of the advanced/metastatic gastric microbiome as a source of diagnostic and targetable biomarkers and its role in modulating responses to immunotherapy. Although Helicobacter pylori (H. pylori) is the most significant risk factor for GC, several other gastrointestinal taxa—including Fusobacterium nucleatum (F. nucleatum)—have been implicated in advanced GC (AGC). At its inception, microbial dysbiosis contributes to chronic inflammation and immune evasion, thereby influencing tumor behavior and treatment efficacy. Integrating microbiome-based biomarkers into risk stratification, GC staging, and targetable treatment frameworks may enhance early detection, inform immunotherapy strategies, and improve patient-specific treatment responses. Bifidobacterium and Lactobacillus rhamnosus GG have the potential to change the immunotherapy framework with their direct influence on dendritic cell (DC) and cytotoxic T cell (CTL) activity. However, clinical translation is impeded by methodological heterogeneity, causality limitations, and a lack of clinical trials. Nonetheless, the integration of microbiome profiling and the development of therapeutic microbiome modulation strategies, such as personalized probiotics regimens and fecal microbiota transplantation, hold substantial potential for improving clinical outcomes and reducing treatment-related toxicity in GC management. Full article

(This article belongs to the Special Issue Molecular Targets in Gastrointestinal Diseases)

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14 pages, 589 KB

Open AccessReview

T Regulatory Cells in Inflammatory Bowel Disease—Are They Major Players?

by Katarzyna Sznurkowska

Int. J. Mol. Sci. 2025, 26(24), 11944; https://doi.org/10.3390/ijms262411944 - 11 Dec 2025

Cited by 1 | Viewed by 1589

Abstract

Inflammatory bowel disease (IBD) is a chronic condition whose pathogenesis is not entirely clear. Impaired immune regulation has been hypothesized as the mechanism responsible for the abnormal response of adoptive immunity to enteric microbial antigens. Regulatory T cells (Tregs) have been regarded as the crucial element of immune regulation, since the discovery that humans lacking Tregs due to mutation of FOXP3 develop autoimmune disorders, including severe bowel inflammation. The existing publications concerning T regulatory cells in human IBD have been reviewed, and current evidence does not clearly indicate quantitative disturbances or functional defects of Tregs in human inflammatory bowel disease. The possible mechanisms explaining immunoregulatory failure in IBD have been summarized. So far, only one clinical trial with Tregs infusion has been completed, and its results do not provide sufficient data on the efficacy or safety of Tregs-based therapies in IBD. It will probably be difficult to implement them in clinical practice in the near future. Full article

(This article belongs to the Special Issue Molecular Targets in Gastrointestinal Diseases)

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17 pages, 2006 KB

Open AccessReview

Targeting NEK Kinases in Gastrointestinal Cancers: Insights into Gene Expression, Function, and Inhibitors

by Lei Chen, Heng Lu, Farah Ballout, Wael El-Rifai, Zheng Chen, Ravindran Caspa Gokulan, Oliver Gene McDonald and Dunfa Peng

Int. J. Mol. Sci. 2025, 26(5), 1992; https://doi.org/10.3390/ijms26051992 - 25 Feb 2025

Cited by 5 | Viewed by 3281

Abstract

Gastrointestinal (GI) cancers, which mainly include malignancies of the esophagus, stomach, intestine, pancreas, liver, gallbladder, and bile duct, pose a significant global health burden. Unfortunately, the prognosis for most GI cancers remains poor, particularly in advanced stages. Current treatment options, including targeted and immunotherapies, are less effective compared to those for other cancer types, highlighting an urgent need for novel molecular targets. NEK (NIMA related kinase) kinases are a group of serine/threonine kinases (NEK1-NEK11) that play a role in regulating cell cycle, mitosis, and various physiological processes. Recent studies suggest that several NEK members are overexpressed in human cancers, including gastrointestinal (GI) cancers, which can contribute to tumor progression and drug resistance. Among these, NEK2 stands out for its consistent overexpression in all types of GI cancer. Targeting NEK2 with specific inhibitors has shown promising results in preclinical studies, particularly for gastric and pancreatic cancers. The development and clinical evaluation of NEK2 inhibitors in human cancers have emerged as a promising therapeutic strategy. Specifically, an NEK2 inhibitor, T-1101 tosylate, is currently undergoing clinical trials. This review will focus on the gene expression and functional roles of NEKs in GI cancers, as well as the progress in developing NEK inhibitors. Full article

(This article belongs to the Special Issue Molecular Targets in Gastrointestinal Diseases)

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