# LncRNA MCF2L-AS1 promotes malignant progression of colorectal cancer by post-transcriptional activation of MCF2L

## TL;DR

This study shows that the lncRNA MCF2L-AS1 promotes colorectal cancer progression by helping to produce the MCF2L protein through a specific molecular mechanism.

## Contribution

The study reveals a novel post-transcriptional regulatory mechanism by which MCF2L-AS1 promotes CRC progression via AUF1-dependent translational activation of MCF2L.

## Key findings

- MCF2L-AS1 is significantly upregulated in colorectal cancer tissues and cells.
- MCF2L-AS1 promotes cancer cell viability, migration, and invasion both in vitro and in vivo.
- MCF2L-AS1 binds to AUF1 to enhance MCF2L protein synthesis independently of mRNA stability.

## Abstract

To elucidate the functional role of MCF2L antisense RNA1 (MCF2L-AS1) in colorectal cancer (CRC) progression and its potential molecular mechanism.

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.

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.

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.

The online version contains supplementary material available at 10.1007/s12672-026-04394-6.