{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE343nnn/GSE343610/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"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=GSE343610"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"MACF1 Promotes Colorectal Cancer Progression via ATF4-Mediated ASNS Regulation","description":"Background: Microtubule-actin cross-linking factor 1 (MACF1) is a cytoskeletal cross-linker implicated in cancer pathogenesis, yet its role in colorectal cancer (CRC) progression remains unclear. This study investigated MACF1 expression, function, and its mechanistic link to the ATF4-ASNS regulatory axis in CRC. Methods: MACF1 expression was assessed in CRC tissues and cell lines (HCT116, HT29, SW620, Caco2, LoVo) via immunohistochemistry and qPCR. Functional assays—including proliferation, colony formation, wound healing, Transwell migration, and cell-cycle analysis—were performed following MACF1 knockdown and overexpression. In vivo tumor growth was evaluated using a subcutaneous xenograft model. RNA-seq screening identified ASNS as a downstream effector, and the MACF1–ATF4–ASNS relationship was explored through ChIP, immunofluorescence, nuclear fractionation, and Co-IP. Results: MACF1 was significantly elevated in CRC tissues and cells versus controls (p < 0.05). MACF1 knockdown suppressed proliferation, colony formation, migration, and xenograft tumor growth, while overexpression promoted aggressive phenotypes (p < 0.05). Mechanistically, ASNS was identified as a critical MACF1 target, with ATF4 serving as a transcriptional mediator linking MACF1 to ASNS regulation. Conclusion: Our findings demonstrate that MACF1 promotes CRC cell growth and migration, at least in part, via ATF4-associated ASNS regulation and asparagine metabolism. This work establishes a novel functional bridge between cytoskeletal remodeling and amino acid metabolic reprogramming in CRC, offering potential insights for future metabolism-oriented therapeutic strategies.","dates":{"publication":"2026/08/17"},"accession":"GSE343610","cross_references":{"GSM":["GSM9958191","GSM9958190","GSM9958193","GSM9958192","GSM9958188","GSM9958189"],"GPL":["24676"],"GSE":["343610"],"taxon":["Homo sapiens"]}}