» Articles » PMID: 34355542

Harness the Functions of Gut Microbiome in Tumorigenesis for Cancer Treatment

Overview
Publisher Wiley
Specialty Oncology
Date 2021 Aug 6
PMID 34355542
Citations 15
Authors
Affiliations
Soon will be listed here.
Abstract

It has been shown that gut microbiota dysbiosis leads to physiological changes and links to a number of diseases, including cancers. Thus, many cancer categories and treatment regimens should be investigated in the context of the microbiome. Owing to the availability of metagenome sequencing and multiomics studies, analyses of species characterization, host genetic changes, and metabolic profile of gut microbiota have become feasible, which has facilitated an exponential knowledge gain about microbiota composition, taxonomic alterations, and host interactions during tumorigenesis. However, the complexity of the gut microbiota, with a plethora of uncharacterized host-microbe, microbe-microbe, and environmental interactions, still contributes to the challenge of advancing our knowledge of the microbiota-cancer interactions. These interactions manifest in signaling relay, metabolism, immunity, tumor development, genetic instability, sensitivity to cancer chemotherapy and immunotherapy. This review summarizes current studies/molecular mechanisms regarding the association between the gut microbiota and the development of cancers, which provides insights into the therapeutic strategies that could be harnessed for cancer diagnosis, treatment, or prevention.

Citing Articles

Oral intake of Hibiscus sabdariffa L. increased c-Myc and caspase-3 gene expression and altered microbial population in colon of BALB/c mice induced to preneoplastic lesions.

Ladeira Bernardes A, Albuquerque Pereira M, Xisto Campos I, Avila L, Dos Santos Cruz B, Duarte Villas Mishima M Eur J Nutr. 2025; 64(3):109.

PMID: 40042671 DOI: 10.1007/s00394-025-03622-z.


Fecal Microbiota Transplantation: Insights into Colon Carcinogenesis and Immune Regulation.

Brusnic O, Onisor D, Boicean A, Hasegan A, Ichim C, Guzun A J Clin Med. 2024; 13(21).

PMID: 39518717 PMC: 11547077. DOI: 10.3390/jcm13216578.


Isobutyric Acid Promotes Immune Evasion in Colorectal Cancer via Increased PD-L1 Expression.

Lin Q, Wang H, Chen W, Wei X, Chen J, Deng Y Cancer Med. 2024; 13(21):e70397.

PMID: 39503247 PMC: 11538990. DOI: 10.1002/cam4.70397.


Friend or Foe: Exploring the Relationship between the Gut Microbiota and the Pathogenesis and Treatment of Digestive Cancers.

Profir M, Rosu O, Cretoiu S, Gaspar B Microorganisms. 2024; 12(5).

PMID: 38792785 PMC: 11124004. DOI: 10.3390/microorganisms12050955.


-induced imbalance in microbiome-derived butyric acid levels promotes the occurrence and development of colorectal cancer.

Wu Q, Fang X, Wan X, Ding Q, Zhang Y, Ji L World J Gastroenterol. 2024; 30(14):2018-2037.

PMID: 38681125 PMC: 11045493. DOI: 10.3748/wjg.v30.i14.2018.


References
1.
Feng Q, Liang S, Jia H, Stadlmayr A, Tang L, Lan Z . Gut microbiome development along the colorectal adenoma-carcinoma sequence. Nat Commun. 2015; 6:6528. DOI: 10.1038/ncomms7528. View

2.
Plovier H, Everard A, Druart C, Depommier C, Van Hul M, Geurts L . A purified membrane protein from Akkermansia muciniphila or the pasteurized bacterium improves metabolism in obese and diabetic mice. Nat Med. 2016; 23(1):107-113. DOI: 10.1038/nm.4236. View

3.
Aykut B, Pushalkar S, Chen R, Li Q, Abengozar R, Kim J . The fungal mycobiome promotes pancreatic oncogenesis via activation of MBL. Nature. 2019; 574(7777):264-267. PMC: 6858566. DOI: 10.1038/s41586-019-1608-2. View

4.
Kao D, Roach B, Silva M, Beck P, Rioux K, Kaplan G . Effect of Oral Capsule- vs Colonoscopy-Delivered Fecal Microbiota Transplantation on Recurrent Clostridium difficile Infection: A Randomized Clinical Trial. JAMA. 2017; 318(20):1985-1993. PMC: 5820695. DOI: 10.1001/jama.2017.17077. View

5.
Pushalkar S, Hundeyin M, Daley D, Zambirinis C, Kurz E, Mishra A . The Pancreatic Cancer Microbiome Promotes Oncogenesis by Induction of Innate and Adaptive Immune Suppression. Cancer Discov. 2018; 8(4):403-416. PMC: 6225783. DOI: 10.1158/2159-8290.CD-17-1134. View