Abstract
PURPOSE: To elucidate the functional role of MCF2L antisense RNA1 (MCF2L-AS1) in colorectal cancer (CRC) progression and its potential molecular mechanism. METHODS: The expression of MCF2L-AS1/MCF2L in CRC cell lines was detected by qRT-PCR. The biological function of MCF2L-AS1 was investigated in vitro and in vivo (colony formation, CCK8, Apoptosis assays, wound healing and transwell assays, and mouse xenograft models). Mechanistic investigations involved bioinformatics analysis followed by experimental validation using Fluorescence in situ hybridization, RNA pull-down, and RNA immunoprecipitation. RESULTS: MCF2L-AS1 was notably upregulated in CRC tissues and cells. Functionally, MCF2L-AS1 suppression markedly attenuated the viability and colony capacity of CRC cells, and the number of migratory and invasive cells was markedly reduced both in vivo and in vitro. Mechanism studies have shown that MCF2L-AS1 binds to the heterogeneous nuclear ribonucleoprotein AUF1, facilitating MCF2L protein synthesis through a post-transcriptional regulatory mechanism independent of mRNA stability. CONCLUSIONS: MCF2L-AS1 promotes CRC progression through AUF1-dependent translational regulation of MCF2L expression. MCF2L-AS1 may represents a potential therapeutic target for clinical intervention in CRC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12672-026-04394-6.