<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/GSE343nnn/GSE343610/</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=GSE343610</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>MACF1 Promotes Colorectal Cancer Progression via ATF4-Mediated ASNS Regulation</name><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 &lt; 0.05). MACF1 knockdown suppressed proliferation, colony formation, migration, and xenograft tumor growth, while overexpression promoted aggressive phenotypes (p &lt; 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.</description><dates><publication>2026/08/17</publication></dates><accession>GSE343610</accession><cross_references><GSM>GSM9958191</GSM><GSM>GSM9958190</GSM><GSM>GSM9958193</GSM><GSM>GSM9958192</GSM><GSM>GSM9958188</GSM><GSM>GSM9958189</GSM><GPL>24676</GPL><GSE>343610</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>