Comprehensive genomics and functional analyses identify SMARCAL1 as a key oncogenic regulator in lung adenocarcinoma

SMARCAL1, a member of the SNF2-family DNA translocases, plays a crucial role in maintaining genomic stability, and its dysregulation may contribute to tumorigenesis. This study investigated the potential of SMARCAL1 as a biomarker in lung adenocarcinoma (LUAD).

Transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets were analyzed to assess SMARCAL1 expression patterns and biological functions. Quantitative polymerase chain reaction (qPCR) confirmed the expression of SMARCAL1 in LUAD tissues, and in vitro assays revealed the impact of SMARCAL1 knockdown on lung cancer cell. Single-sample gene set enrichment analysis was employed to explore the correlations between SMARCAL1 and immune cell infiltration. Furthermore, tumor mutational burden (TMB) and therapeutic response analyses indicated that SMARCAL1 expression was associated with TMB and differential sensitivity to targeted and immunotherapeutic agents. The study also employed a prognostic model integrating SMARCAL1 expression levels to predict patient outcomes.

SMARCAL1 demonstrates elevated expression levels in LUAD, exhibiting a correlation with its tumor size, lymph node involvement and metastasis (TNM) stage. Furthermore, the proliferation, migration, and invasion capabilities of LUAD cells were found to be inhibited following the knockdown of SMARCAL1. We constructed a prognostic model of LUAD, which exhibited a substantial predictive capacity in predicting patients' survival rates. Concurrently, we ascertained that patients exhibiting high SMARCAL1 expression may possess diminished anti-tumor immunity and elevated tumor mutation load.

SMARCAL1 plays a pivotal role in the development of LUAD and exhibits promise in predicting the prognosis and therapeutic efficacy of this malignancy. It is a promising candidate for utilization as a biomarker for LUAD.