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Cells
Special Issues
Gastrointestinal Disease: From Cellular Mechanisms to Targeted Therapy
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Gastrointestinal Disease: From Cellular Mechanisms to Targeted Therapy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 7386

Special Issue Editors

Dr. Grazia Serino

E-Mail Website1 Website2
Guest Editor
National Institute of Gastroenterology “S. De Bellis” Research Hospital, Castellana Grotte, Italy
Interests: microRNA; inflammatory bowel disease; gastrointestinal cancer; intestinal permeability
Special Issues, Collections and Topics in MDPI journals
Dr. Amilcare Barca

E-Mail Website
Guest Editor
Laboratory of Applied Physiology, Department of Experimental Medicine, University of Salento, Campus Ecotekne, 73100 Lecce, Italy
Interests: GI cell physiology and pathophysiology; homeostasis mechanisms; transepithelial and transmembrane transport processes; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The pathophysiology of the GI tract includes a broad range of diseases and processes, from injury and repair to chronic inflammatory states and cancer. In recent years, biomedical research has aimed to characterize and elucidate the cellular mechanisms underlying GI disease progression. New technologies that focus on genomic, transcriptomic, and proteomic aspects allow us to identify the molecular mechanisms that drive disease onset and progression and thus new potential targets for therapy.

This Special Issue will aim to cover novel research exploring all cellular mechanisms, ranging from the induction of apoptosis and autophagy to cell cycle arrest, epithelial turnover, inhibition of epithelial–mesenchymal transition, suppression of cellular invasion and migration, and modulation of multiple signaling pathways in gastrointestinal disease, including cancer, immune disease, and infectious disease. Additionally, this Special Issue will include studies that highlight innovative molecular-based drug targets and their associated predictive biomarkers. Original research articles and reviews are welcome.

Dr. Grazia Serino
Dr. Amilcare Barca
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. Cells 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 2700 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

  • gastrointestinal cancer
  • gastric cancer
  • colorectal cancer
  • esophageal cancer
  • liver cancer
  • pancreatic cancer
  • inflammatory bowel disease
  • miRNAs
  • in vitro and in vivo models
  • molecular networks
  • molecular pathways
  • translational medicine
  • epithelial barrier functions/processes

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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16 pages, 1758 KiB  
Article
Molecular Mechanisms of Skatole-Induced Inflammatory Responses in Intestinal Epithelial Caco-2 Cells: Implications for Colorectal Cancer and Inflammatory Bowel Disease
by Katsunori Ishii, Kazuma Naito, Dai Tanaka, Yoshihito Koto, Koichi Kurata and Hidehisa Shimizu
Cells 2024, 13(20), 1730; https://doi.org/10.3390/cells13201730 - 18 Oct 2024
Cited by 1 | Viewed by 1585
Abstract
Inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), in intestinal epithelial cells significantly contribute to inflammatory bowel disease (IBD) and colorectal cancer (CRC). Given our previous findings that TNF-α is upregulated in intestinal epithelial Caco-2 cells induced by skatole, a [...] Read more.
Inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), in intestinal epithelial cells significantly contribute to inflammatory bowel disease (IBD) and colorectal cancer (CRC). Given our previous findings that TNF-α is upregulated in intestinal epithelial Caco-2 cells induced by skatole, a tryptophan-derived gut microbiota metabolite, the present study aimed to explore the relationship between skatole and IL-6, alongside TNF-α. Skatole elevated the promoter activity of IL-6 as well as TNF-α, and increased IL-6 mRNA expression and protein secretion. In addition to activating NF-κB, the NF-κB inhibitor BAY 11-7082 reduced skatole-induced cell survival and the mRNA expression of IL-6 and TNF-α. NF-κB activation was attenuated by the extracellular signal-regulated kinase (ERK) pathway inhibitor U0126 and the p38 inhibitor SB203580, but not by the c-Jun N-terminal kinase (JNK) inhibitor SP600125. U126 and SB203580 also decreased the skatole-induced increase in IL-6 expression. When skatole-induced AhR activation was inhibited by CH223191, in addition to promoting NF-κB activation, IL-6 expression was enhanced in a manner similar to that previously reported for TNF-α. Taken together, these results suggest that skatole-elicited NF-κB activation induces IL-6 and TNF-α expression, although AhR activation partially suppresses this process. The ability of skatole to increase the expression of IL-6 and TNF-α may significantly affect the development and progression of these diseases. Moreover, the balance between NF-κB and AhR activation appears to govern the skatole-induced increases in IL-6 and TNF-α expression. Therefore, the present findings provide new insights into the mechanisms linking tryptophan-derived gut microbiota metabolites with colorectal disease. Full article
(This article belongs to the Special Issue Gastrointestinal Disease: From Cellular Mechanisms to Targeted Therapy)
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29 pages, 7405 KiB  
Article
Immunological Strategies in Gastric Cancer: How Toll-like Receptors 2, -3, -4, and -9 on Monocytes and Dendritic Cells Depend on Patient Factors?
by Marek Kos, Krzysztof Bojarski, Paulina Mertowska, Sebastian Mertowski, Piotr Tomaka, Łukasz Dziki and Ewelina Grywalska
Cells 2024, 13(20), 1708; https://doi.org/10.3390/cells13201708 - 16 Oct 2024
Cited by 1 | Viewed by 1522
Abstract
(1) Introduction: Toll-like receptors (TLRs) are key in immune response by recognizing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). In gastric cancer (GC), TLR2, TLR3, TLR4, and TLR9 are crucial for modulating immune response and tumor progression. (2) Objective: This study [...] Read more.
(1) Introduction: Toll-like receptors (TLRs) are key in immune response by recognizing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). In gastric cancer (GC), TLR2, TLR3, TLR4, and TLR9 are crucial for modulating immune response and tumor progression. (2) Objective: This study aimed to assess the percentage of dendritic cells and monocytes expressing TLR2, TLR3, TLR4, and TLR9, along with the concentration of their soluble forms in the serum of GC patients compared to healthy volunteers. Factors such as disease stage, tumor type, age, and gender were also analyzed. (3) Materials and Methods: Blood samples from newly diagnosed GC patients and healthy controls were immunophenotyped using flow cytometry to assess TLR expression on dendritic cell subpopulations and monocytes. Serum-soluble TLRs were measured by ELISA. Statistical analysis considered clinical variables such as tumor type, stage, age, and gender. (4) Results: TLR expression was significantly higher in GC patients, except for TLR3 on classical monocytes. Soluble forms of all TLRs were elevated in GC patients, with significant differences based on disease stage but not tumor type, except for serum TLR2, TLR4, and TLR9. (5) Conclusions: Elevated TLR expression and soluble TLR levels in GC patients suggest a role in tumor pathogenesis and progression, offering potential biomarkers and therapeutic targets. Full article
(This article belongs to the Special Issue Gastrointestinal Disease: From Cellular Mechanisms to Targeted Therapy)
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Review

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24 pages, 2024 KiB  
Review
Advancements in Utilizing Natural Compounds for Modulating Autophagy in Liver Cancer: Molecular Mechanisms and Therapeutic Targets
by Md Ataur Rahman, S M Rakib-Uz-Zaman, Somdeepa Chakraborti, Sujay Kumar Bhajan, Rajat Das Gupta, Maroua Jalouli, Md. Anowar Khasru Parvez, Mushfiq H. Shaikh, Ehsanul Hoque Apu, Abdel Halim Harrath, Seungjoon Moon and Bonglee Kim
Cells 2024, 13(14), 1186; https://doi.org/10.3390/cells13141186 - 12 Jul 2024
Cited by 1 | Viewed by 3460
Abstract
Autophagy, an intrinsic catabolic mechanism that eliminates misfolded proteins, dysfunctional organelles, and lipid droplets, plays a vital function in energy balance and cytoplasmic quality control, in addition to maintaining cellular homeostasis. Liver cancer such as hepatocellular carcinoma (HCC) is one of the most [...] Read more.
Autophagy, an intrinsic catabolic mechanism that eliminates misfolded proteins, dysfunctional organelles, and lipid droplets, plays a vital function in energy balance and cytoplasmic quality control, in addition to maintaining cellular homeostasis. Liver cancer such as hepatocellular carcinoma (HCC) is one of the most common causes of cancer deaths globally and shows resistance to several anticancer drugs. Despite the rising incidence and poor prognosis of malignant HCC, the underlying molecular mechanisms driving this aggressive cancer remain unclear. Several natural compounds, such as phytochemicals of dietary and non-dietary origin, affect hepatocarcinogenesis signaling pathways in vitro and in vivo, which may help prevent and treat HCC cells. Current HCC cells treatments include chemotherapy, radiation, and surgery. However, these standard therapies have substantial side effects, and combination therapy enhances side effects for an acceptable therapeutic benefit. Therefore, there is a need to develop treatment strategies for HCC cells that are more efficacious and have fewer adverse effects. Multiple genetic and epigenetic factors are responsible for the HCC cells to become resistant to standard treatment. Autophagy contributes to maintain cellular homeostasis, which activates autophagy for biosynthesis and mitochondrial regulation and recycling. Therefore, modifying autophagic signaling would present a promising opportunity to identify novel therapies to treat HCC cells resistant to current standard treatments. This comprehensive review illustrates how natural compounds demonstrate their anti-hepatocellular carcinoma function through autophagy. Full article
(This article belongs to the Special Issue Gastrointestinal Disease: From Cellular Mechanisms to Targeted Therapy)
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