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. 2022 Aug 12;12:897330. doi: 10.3389/fonc.2022.897330

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Copyright © 2022 Zhu, Wang, Liu and Wei

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Overview of proposed mechanisms that Fusobacterium nucleatum invading cancer cells. F. nucleatum is a common bacterium in the oral cavity. F. nucleatum invades ESCC cells and CRC cells. F. nucleatum may transfer through lymph, vessel, or direct diffusion. F. nucleatum promotes ESCC progression by the NOD1/RIPK2/NFκB pathway. FadA is highly conserved among F. nucleatum and expressed on the bacterial surface. FadA binds E-cadherin on CRC cells to attach and invade CRC cells. Then, NFκB signaling and β-catenin signaling are activated to induce a pro-inflammatory cascade to promote CRC progression. ESCC, esophageal squamous cell carcinoma; CRC, colorectal cancer; Fn, Fusobacterium nucleatum; NOD1, nucleotide-binding oligomerization domain-containing protein 1; RIPK2, interacting serine threonine kinase 2; NFκB, nuclear factor-κB.