ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
A20 Facilitates Oxaliplatin Sensitivity in Colorectal Cancer Through Monoubiquitylation of IKK-β.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
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13 authors.
Funding
Abstract
The ubiquitin-editing enzyme A20 is essential for maintaining inflammatory homeostasis, yet its role in chemoresistance remains unclear. To investigate how A20 regulates oxaliplatin resistance in colorectal cancer (CRC), with a focus on A20-mediated IKK-β monoubiquitylation at K163. A prospective, randomized Phase III study is conducted in patients with locally advanced CRC who received either oxaliplatin+capecitabine neoadjuvant chemoradiotherapy (oxaliplatin-NACRT) or capecitabine-only neoadjuvant chemoradiotherapy (non-oxaliplatin-NACRT). Preoperative biopsy and matched surgical specimens are evaluated by immunohistochemistry to determine A20's association with oxaliplatin response. In oxaliplatin-NACRT group, patients achieving pathological complete response (pCR) displayed lower A20 expression than non-pCR patients, whereas no difference is observed in non-oxaliplatin-NACRT group. Two additional independent cohorts confirmed A20 downregulation in human CRC tissues, and reduced A20 expression correlated with poorer survival and oxaliplatin resistance. Mechanistically, A20 monoubiquitylates IKK-β via its fourth zinc-finger domain, promoting IKK-β degradation and suppressing NF-κB nuclear translocation. A20 knockdown or expression of the IKK-β K163R mutant induced oxaliplatin resistance in mouse xenografts. Clinically, A20 expression are negatively associated with IKK-β and its downstream targets. A20 depletion promotes oxaliplatin resistance in CRC by stabilizing IKK-β. the results uncover an essential role of the A20-IKK-β axis in oxaliplatin resistance of CRC.
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