Targeting Programmed Fusobacterium nucleatum Fap2 for Colorectal Cancer Therapy

Abstract

Colorectal patients generally have the maximum counts of Fusobacterium nucleatum (F. nucleatum) in tumors and elevate colorectal adenomas and carcinomas, which show the lowest rate of human survival. Hence, F. nucleatum is a diagnostic marker of colorectal cancer (CRC). Studies demonstrated that targeting fusobacterial Fap2 or polysaccharide of the host epithelium may decrease fusobacteria count in the CRC. Attenuated F. nucleatum-Fap2 prevents transmembrane signals and inhibits tumorigenesis inducing mechanisms. Hence, in this review, we hypothesized that application of genetically programmed fusobacterium can be skillful and thus reduce fusobacterium in the CRC. Genetically programmed F. nucleatum is a promising antitumor strategy.

Keywords: CRC; Fusobacterium nucleatum; cancer therapy; genetically programmed.

Figure 1

Migration of F. nucleatum from the oral cavity to colon that promote colorectal cancer (CRC).

Figure 2

Programmed/attenuated F. nucleatum Fap2 as a potent factor for the treatment of CRC. Abbreviation: Akt-protein kinase B; Ap1-activating protein-1; ERK-extracellular signal-regulated kinase; FadA- Fusobacterium adhesin A; Fap2-fibroblast activation protein 2; Gal-GalNAc-acetylgalactosamine; IkB-Ikappa B proteins; IKK-Ikappa B kinase; IRAK1-Interleukin-1; receptor-associated kinase 1; IRAK4-Interleukin-1 receptor-associated kinase 4; LPS-lipopolysaccharide; MAPK-mitogen-activated protein kinase; MEK-MAPK-ERK-kinase; mTOR-mammalian target of rapamycin; MYD88-myeloid differentiation primary response gene 88; NF-kB-nuclear factor kappa-B; p-phosphorylated; PI3K-phosphatidylinositol 3-kinase; RAF-rapidly accelerated fibrosarcoma; RAS-rat sarcoma; TLR4-Toll-like receptor 4; TRAF6-Tumor necrosis factor receptor associated factor 6; TRAM-Transverse rectus abdominis myocutaneous; TRAP-thyroid hormone receptor associated protein.