Published online Apr 14, 2024. doi: 10.3748/wjg.v30.i14.2018
Peer-review started: October 31, 2023
First decision: December 15, 2023
Revised: January 11, 2024
Accepted: February 29, 2024
Article in press: February 29, 2024
Published online: April 14, 2024
Processing time: 164 Days and 10.5 Hours
Colorectal cancer (CRC) ranks among the most prevalent malignant neoplasms globally. Fusobacterium nucleatum (F. nucleatum) has been implicated in the initiation, progression, and prognostic outcomes of CRC. Butyrate, a short-chain fatty acid (SCFA) derived from the bacterial fermentation of soluble dietary fiber, exhibits inhibitory effects on several types of cancers.
Recent research has demonstrated that the SCFA butyrate can suppress the proliferation, enrichment, and adherence of F. nucleatum in CRC tissues. This suppression is achieved by the downregulation of adhesion-associated outer membrane proteins, including RadD, FomA, and FadA. Consequently, this leads to a decrease in the colonization and invasion of F. nucleatum and mitigates its contribution to chemoresistance. Therefore, this study aims to investigate whether F. nucleatum can influence the synthesis of the intestinal metabolite butyric acid, thereby facilitating the development of CRC.
Exploring whether F. nucleatum affects the production of intestinal metabolite butyrate to promote CRC development.
Fecal samples were collected from mice in the treatment group following oral administration of F. nucleatum for the analysis of SCFAs and 16S rDNA. Concurrently, CRC cells underwent co-treatment with F. nucleatum and sodium butyrate (NaB) in vitro to assess alterations in the cell cycle, mitochondrial functionality, and the expression of pertinent proteins.
The abundance of F. nucleatum is markedly elevated in fecal specimens and CRC tissues from patients with CRC. F. nucleatum suppresses the synthesis of the SCFA butyric acid. NaB impairs mitochondrial functionality and impedes the cell cycle in CRC cells. Both NaB and F. nucleatum modulate the growth of CRC cells via the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. The presence of AMPK is essential for NaB’s effectiveness in inhibiting CRC cell proliferation.
Our findings showed that the abundance of F. nucleatum is significantly high in fecal samples and CRC tissues from CRC patients. F. nucleatum impedes the synthesis of the SCFA butyric acid. NaB compromises mitochondrial functionality and obstructs the cell cycle in CRC cells. The growth of CRC cells is modulated by both NaB and F. nucleatum via the AMPK signaling pathway. The presence of AMPK is critical for the ability of NaB to curb CRC cell proliferation.
The outcomes of this research could enhance our comprehension of CRC pathogenesis, potentially leading to the formulation of more efficacious therapeutic strategies.