<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE338nnn/GSE338053/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE338053</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>3-Hydroxyanthranilic acid suppresses colorectal cancer growth and enhances 5-fluorouracil sensitivity via the YY1–p53 and YY1–DKK4 axes [RNA-Seq 3HAA_5FU_HCT116]</name><description>In spite of its reported tumor-growth-inhibition activity, the role of the tryptophan metabolite 3-hydroxyanthranilic acid (3-HAA) in colorectal cancer (CRC) remains unclear. Here, 3-HAA exhibited depleted levels in CRC tissues, and its exogenous administration effectively suppressed the proliferation of multiple CRC cell lines. Through its binding to the Yin Yang 1 (YY1) transcription factor, it disrupted the YY1–p53 interaction, preserved p53 stability, and induced cell cycle arrest. Notably, in vitro, 3-HAA reduced chemoresistance to the common CRC-chemotherapy drug 5-fluorouracil (5-FU) via the YY1–DKK4 axis. Consistently, in vivo, combined 3-HAA–5-FU treatment effectively inhibited CRC progression, highlighting the potential of 3-HAA for CRC therapy.</description><dates><publication>2026/09/11</publication></dates><accession>GSE338053</accession><cross_references><GSM>GSM9865380</GSM><GSM>GSM9865378</GSM><GSM>GSM9865377</GSM><GSM>GSM9865379</GSM><GSM>GSM9865374</GSM><GSM>GSM9865373</GSM><GSM>GSM9865376</GSM><GSM>GSM9865375</GSM><GPL>34284</GPL><GSE>338053</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>