<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Luo F</submitter><funding>Fundamental Research Funds for the Central Universities, Sun Yat-sen University</funding><funding>Natural Science Foundation of Guangdong Province</funding><funding>China Postdoctoral Science Foundation</funding><funding>National Natural Science Foundation of China</funding><funding>Fostering Program for NSFC Young Applicants (Tulip Talent Training Program) of Sun Yat-sen University Cancer Center</funding><funding>Young Talents Program of Sun Yat-sen University Cancer Center</funding><pagination>e14486</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12948199</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(12)</volume><pubmed_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 e</pubmed_abstract><journal>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</journal><pubmed_title>A20 Facilitates Oxaliplatin Sensitivity in Colorectal Cancer Through Monoubiquitylation of IKK-β.</pubmed_title><pmcid>PMC12948199</pmcid><funding_grant_id>YTP-SYSUCC-0104</funding_grant_id><funding_grant_id>2024M753753</funding_grant_id><funding_grant_id>82 303 807</funding_grant_id><funding_grant_id>24qnpy283</funding_grant_id><funding_grant_id>2024A1515013011</funding_grant_id><funding_grant_id>82 203 649</funding_grant_id><funding_grant_id>2025yfd18</funding_grant_id><funding_grant_id>82 473 398</funding_grant_id><pubmed_authors>Chen Q</pubmed_authors><pubmed_authors>Xia Z</pubmed_authors><pubmed_authors>Cao J</pubmed_authors><pubmed_authors>Lu Z</pubmed_authors><pubmed_authors>Luo F</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Lu F</pubmed_authors><pubmed_authors>Zhang R</pubmed_authors><pubmed_authors>Ma W</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>Lin C</pubmed_authors><pubmed_authors>Luo M</pubmed_authors><pubmed_authors>Yang T</pubmed_authors></additional><is_claimable>false</is_claimable><name>A20 Facilitates Oxaliplatin Sensitivity in Colorectal Cancer Through Monoubiquitylation of IKK-β.</name><description>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 e</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Feb</publication><modification>2026-07-16T22:20:31.506Z</modification><creation>2026-07-11T03:12:11.776Z</creation></dates><accession>S-EPMC12948199</accession><cross_references><pubmed>41405367</pubmed><doi>10.1002/advs.202514486</doi></cross_references></HashMap>