Relevance of STK11 Mutations Regarding Immune Cell Infiltration, Drug Sensitivity, and Cellular Processes in Lung

Zhenqing Li1,2, Bo Ding1,2, Jianxun Xu1,2

  • 1Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China.

Frontiers in Oncology
|January 11, 2021
PubMed

Insights

Serine/threonine kinase 11 (STK11) mutations occur in 19% of lung adenocarcinoma (LUAD) cases, impacting immune infiltration and potentially responding to Nutlin-3a(-). These findings offer targets for personalized LUAD treatment.

Area of Science:

  • Oncology
  • Genomics
  • Molecular Biology

Background:

  • Serine/threonine kinase 11 (STK11) is a tumor suppressor involved in cell polarity, apoptosis, and DNA repair.
  • STK11 mutations are prevalent in lung adenocarcinoma (LUAD), influencing tumor behavior.

Purpose of the Study:

  • To investigate the relevance of STK11 mutations in LUAD.
  • To analyze the correlation between STK11 mutations, immune cell infiltration, drug sensitivity, and cellular processes.

Main Methods:

  • Bioinformatic analysis of The Cancer Genome Atlas (TCGA) LUAD patient data.
  • Differential gene expression analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Ontology (GO) enrichment.
  • Genomics of Drug Sensitivity in Cancer (GDSC) data analysis for drug sensitivity.

Main Results:

  • STK11 mutations were found in approximately 19% of LUAD patients.
  • 746 differentially expressed genes (DEGs) were identified, enriched in tumorigenesis and metabolic pathways.
  • LUAD patients with STK11 mutations exhibited lower immune cell infiltration, correlated with STK11 gene copy number.
  • Nutlin-3a(-) emerged as a potential sensitive drug for LUAD with STK11 mutations.

Conclusions:

  • STK11 mutations significantly impact LUAD characteristics, including immune infiltration and cellular processes.
  • Identifying specific genes and pathways associated with STK11 mutations can guide individualized LUAD treatment strategies.
  • Nutlin-3a(-) shows promise as a targeted therapy for LUAD patients with STK11 mutations.

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