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Figure 3. 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.