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. 2023 Feb 1;34(2):227-237.
doi: 10.1097/CAD.0000000000001413. Epub 2023 Oct 24.

Butyrate ameliorates colorectal cancer through regulating intestinal microecological disorders

Jingjing Kang  1 , Mingzhong Sun  2 , Yi Chang  2 , Hongmei Chen  2 , Juan Zhang  2 , Xiaodong Liang  3 , Tengfei Xiao  2
Affiliations

Butyrate ameliorates colorectal cancer through regulating intestinal microecological disorders

Jingjing Kang et al. Anticancer Drugs. .

Abstract

The occurrence and progression of colorectal cancer (CRC) are closely related to intestinal microecological disorders. Butyrate, the representative of short chain fatty acids, possess anti-inflammatory and antioxidant effects, and its antitumor effect has been gradually paid attention to. In this study, azoxymethane/dextran sodium sulfate induced mouse CRC model was used to explore the role and mechanism of butyrate in regulating colon cancer and its intestinal microecological balance. Outcomes exhibited that butyrate alleviated weight loss, disease activity index, and survival in CRC mice and inhibited tumor number and progression. Further research revealed that butyrate restrained the aggregation of harmful while promoting the colonization of beneficial flora, such as Actinobacteriota, Bifidobacteriales and Muribaculacea through 16S rDNA sequence analysis. This study confirmed that butyrate can ameliorate CRC by repairing intestinal microecology, providing ideas and evidence for chemical prophylactic agents, such as butyrate to remedy tumors and regulate tumor microbiota.

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Conflict of interest statement

There are no conflicts of interest.

Figures

Fig. 1
Fig. 1
Butyrate relieves symptoms of AOM/DSS induced CAC. (a) Protocol of AOM/DSS induced CAC. (b) The body weight loss (n = 10 per group). (c) The disease activity index (DAI) (n = 10 per group). (d) Survival curve analysis (n = 10 per group). (e) The rectal prolapse of mice at the 10th week. Data are represented as the mean ± standard. *P < 0.05. AOM/DSS, azoxymethane-dextran sodium sulfate; CAC, colitis-associated colorectal cancer.
Fig. 2
Fig. 2
Butyrate attenuated the occurrence and progression of CRC. (a) Macroscopic morphology of colon tumors. (b) The number of colon tumors (n = 10 per group). (c) Macroscopic morphology of spleen. (d) The weight of spleen (n = 10 per group). (e) Hematoxylin-eosin (H&E) staining of colon and spleen (microscope ×40). (f) Histological score (n = 10 per group). Data are represented as the mean ± standard. *P < 0.05. CRC, colorectal cancer.
Fig. 3
Fig. 3
Butyrate changed gut flora diversity in CRC mice. (a) The ACE index. (b) The Chao 1 estimator. (c) The Shannon index. (d) The Simpson index. (e) Good’s coverage index. Data are represented as the mean ± standard. *P < 0.05, **P < 0.01 and ***P < 0.001. CRC, colorectal cancer.
Fig. 4
Fig. 4
Butyrate influenced on gut microbiota community composition in CRC mice. (a) The ANOSIM index. (b) PCA of β diversity. (c) PCoA of β diversity. (d) NMDS analysis. ANOSIM, analysis of similarities; CRC, colorectal cancer; NMDS, Non-metric multidimensional scaling; PCA, principal co-ordinates analysis; PcoA, principal co-ordinates analysis.
Fig. 5
Fig. 5
Butyrate restored gut microecological dysbiosis in CRC mice. Relative abundance analysis at (a) phylum level; (b) class level; (c) order level; (d) family level; (e) genus level; (f) species level among three groups. CRC, colorectal cancer.
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