{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE338nnn/GSE338053/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE338053"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"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]","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.","dates":{"publication":"2026/09/11"},"accession":"GSE338053","cross_references":{"GSM":["GSM9865380","GSM9865378","GSM9865377","GSM9865379","GSM9865374","GSM9865373","GSM9865376","GSM9865375"],"GPL":["34284"],"GSE":["338053"],"taxon":["Homo sapiens"]}}