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. 2022 May 12;5(2):436–450. doi: 10.20517/cdr.2021.144

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© The Author(s) 2022.

© The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Specific mechanisms of drug resistance induced by Fn. The research on Fn-mediated drug resistance mainly focuses on autophagy activation (A,B) and apoptosis blockade (C-F). (A) Fn modulates endogenous LC3 and ATG7 expression to induce chemoresistance against 5-FU, CDDP, and docetaxel in ESCC. (B) Fn intervention induces a selective loss of miR-4802 and miR-18a*, leading to TLR4/MYD88-dependent autophagy activation and a CRC chemotherapeutic response to OXA and 5-FU. (C) Fn-mediated TLR4/MYD88/NF-κB pathway activation induces upregulation of BIRC3, which consequently cripples the level of cleaved caspase 3 and cleaved PARP caused by 5-FU. (D) In colon cancer cells, the apoptosis effects induced by OXA and 5-FU could be prevented by Fn-induced ANO1 upregulation. (E) Fn-induced overexpression of ANXA1 confers 5-FU resistance in colon cancer cells, but the specific mechanism needs further investigation. (F) Fn may downregulate p53 expression through the non-canonical Wnt/NFAT pathway to inhibit CDDP-induced apoptosis and migration in OSCC cells. Fn: Fusobacterium nucleaum; 5-FU: 5-fluorouracil; OXA: oxaliplatin; CRC: colorectal cancer; CDDP: cisplatin; ESCC: esophageal squamous cell carcinoma; BIRC3: baculoviral IAP repeat-containing protein 3; ANO1: Anoctamin-1; ANXA1: Annexin A1; OSCC: oral squamous cell carcinoma; PARP: poly ADP-ribose polymerase.