# RECQL4 promotes the malignant progression of lung adenocarcinoma through the YBX1/G3BP1-mediated NF-κB signaling pathway

## TL;DR

This study shows that the RECQL4 protein promotes lung adenocarcinoma progression by activating a specific signaling pathway, suggesting it could be a new target for treatment.

## Contribution

The study identifies a novel molecular mechanism by which RECQL4 promotes lung adenocarcinoma through the YBX1/G3BP1-mediated NF-κB pathway.

## Key findings

- RECQL4 is overexpressed in lung adenocarcinoma tissues and correlates with poor prognosis.
- RECQL4 activates the NF-κB signaling pathway by enhancing the interaction between YBX1 and G3BP1.
- Inhibiting RECQL4 reduces LUAD cell proliferation, migration, and invasion.

## Abstract

Lung adenocarcinoma (LUAD) remains a major global health issue characterized by high incidence and mortality rates. RecQ-like helicase 4 (RECQL4), a member of the DNA helicase family, plays a crucial role in DNA replication, DNA damage repair, and tumor progression. However, its involvement and specific molecular mechanisms in LUAD progression have not been elucidated. Through this investigation, we found that RECQL4 expression was aberrantly elevated in clinical LUAD tissues, and higher levels of RECQL4 expression were associated with poor prognosis and worse clinicopathological characteristics in LUAD patients. Gain-of-function and loss-of-function studies demonstrated that RECQL4 promoted the proliferation, migration, and invasion abilities of LUAD cells. Subsequent gene set enrichment analysis (GSEA) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis confirmed that RECQL4 activates the NF-κB signaling pathway. Mechanistic investigation indicated that RECQL4 might function as a scaffold protein for the Y box binding protein 1 (YBX1) and GTPase-activating protein SH3 domain-binding protein 1 (G3BP1), enhancing the interaction between YBX1 and G3BP1, thereby activating the NF-κB signaling pathway and promoting the progression of LUAD. In conclusion, RECQL4 promotes the malignant progression of LUAD through the YBX1/G3BP1-mediated NF-κB signaling pathway. These findings suggest that RECQL4 has the potential to serve as a novel prognostic biomarker and an effective therapeutic target for LUAD.