Gut Microbiome, Diet and Cancer Risk

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Epidemiology and Prevention".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 622

Special Issue Editor


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Guest Editor
Sydney Medical School, University of Sydney, Sydney, NSW 2065, Australia
Interests: gut microbiome; lifestyle medicine; supportive care in cancer, integrative medicine, Tai Chi Qigong mind-body medicine
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Special Issue Information

Dear Colleagues,

The human gut microbiome—a diverse community of trillions of microorganisms residing in the gastrointestinal tract—plays a critical role in maintaining health and modulating disease risk. Emerging research has revealed a complex interplay between the gut microbiome, dietary patterns, and the development of cancer. Diet is a key determinant of the microbiome’s composition and function, influencing microbial diversity, metabolite production, and inflammatory responses. Specific dietary components, such as fiber, red and processed meats, and polyphenols, can either promote a beneficial microbiota profile or contribute to dysbiosis, a state of microbial imbalance linked to carcinogenesis. Altered microbiota can influence the risk of cancer through mechanisms such as immune modulation, the production of carcinogenic compounds, and epigenetic regulation. Understanding how diet–microbiome interactions affect a person’s cancer risk opens up promising avenues for discovering new preventive and therapeutic strategies. This Special Issue explores the emerging evidence connecting the gut microbiome to dietary influences and their collective impact on cancer development.

Dr. Byeongsang Oh
Guest Editor

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Keywords

  • gut microbiome
  • cancer
  • diet
  • dysbiosis
  • immunity
  • dietary fiber
  • probiotic
  • short-chain fatty acids (SCFAs)

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Published Papers (1 paper)

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Research

30 pages, 10270 KiB  
Article
Fuelling the Fight from the Gut: Short-Chain Fatty Acids and Dexamethasone Synergise to Suppress Gastric Cancer Cells
by Radwa A. Eladwy, Mohamed Fares, Dennis Chang, Muhammad A. Alsherbiny, Chun-Guang Li and Deep Jyoti Bhuyan
Cancers 2025, 17(15), 2486; https://doi.org/10.3390/cancers17152486 - 28 Jul 2025
Viewed by 457
Abstract
Background: Short-chain fatty acids (SCFAs), microbial metabolites also known as postbiotics, are essential for maintaining gut health. However, their antiproliferative effects on gastric cancer cells and potential interactions with conventional therapies remain underexplored. This study aimed to investigate the effects of three SCFA [...] Read more.
Background: Short-chain fatty acids (SCFAs), microbial metabolites also known as postbiotics, are essential for maintaining gut health. However, their antiproliferative effects on gastric cancer cells and potential interactions with conventional therapies remain underexplored. This study aimed to investigate the effects of three SCFA salts—magnesium acetate (A), sodium propionate (P), and sodium butyrate (B)—individually and in combination (APB), as well as in combination with dexamethasone (Dex), on AGS gastric adenocarcinoma cells. Methods: AGS cells were treated with PB, AP, AB, APB, Dex, and APB+Dex. Cell viability was assessed to determine antiproliferative effects, and the IC50 of APB was calculated. Flow cytometry was used to evaluate apoptosis and necrosis. Reactive oxygen species (ROS) levels were measured to assess oxidative stress. Proteomic analysis via LC-MS was performed to identify differential protein expression and related pathways impacted by the treatments. Results: SCFA salts showed significant antiproliferative effects on AGS cells, with APB exhibiting a combined IC50 of 568.33 μg/mL. The APB+Dex combination demonstrated strong synergy (combination index = 0.76) and significantly enhanced growth inhibition. Both APB and APB+Dex induced substantial apoptosis (p < 0.0001) with minimal necrosis. APB alone significantly increased ROS levels (p < 0.0001), while Dex moderated this effect in the combination group APB+Dex (p < 0.0001). Notably, the APB+Dex treatment synergistically targeted multiple tumour-promoting mechanisms, including the impairment of redox homeostasis through SLC7A11 suppression, and inhibition of the haemostasis, platelet activation network and NF-κB signalling pathway via downregulation of NFKB1 (−1.34), exemplified by increased expression of SERPINE1 (1.99) within the “Response to elevated platelet cytosolic Ca2+” pathway. Conclusions: These findings showed a multifaceted anticancer mechanism by APB+Dex that may collectively impair cell proliferation, survival signalling, immune modulation, and tumour microenvironment support in gastric cancer. Full article
(This article belongs to the Special Issue Gut Microbiome, Diet and Cancer Risk)
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