Heat shock factor 2-binding protein promotes tumor progression via activation of MAPK signaling pathway in lung adenocarcinoma.

Lung adenocarcinoma (LUAD) is a malignant tumor that causes a serious public health burden. The biological functions and potential mechanism of heat shock factor 2-binding protein (HSF2BP) in LUAD have not been studied. This study aimed to explore the HSF2BP expression pattern and its potential biological function in LUAD. The transcriptome data and relevant clinical data of LUAD were downloaded from The Cancer Genome Atlas (TCGA) database. The mRNA levels and prognosis of HSF2BP were determined using TCGA datasets. The protein and mRNA expression levels of HSF2BP were identified by conducting western blot analysis and quantitative real-time polymerase chain reaction in tissues and cells, respectively. To determine whether HSF2BP affected the biological function of LUAD cell lines, a series of functional experiments were performed in vitro and in vivo. In addition, gene set enrichment analysis was applied to determine the pathways that HSF2BP regulated, which was further confirmed by western blotting, and the high expression of HSF2BP was observed in LUAD, which was correlated with the unfavorable prognosis in LUAD patients. Clinical correlation analysis revealed that tumor stage was positively correlated with high HSF2BP expression. Furthermore, HSF2BP could serve as an independent risk factor for overall survival. In vitro, HSF2BP knockdown suppressed the proliferation and migration of A549 and H1299 cells. We observed the same results in vivo experiments. Mechanistically, the HSF2BP regulates the mitogen-activated protein kinase signaling pathway to perform its biological function. The HSF2BP plays a role in the development of LUAD and could be a useful anticancer target for the treatment of LUAD.