Maintains Cancer Stemness and Promotes Erlotinib Resistance in Lung Adenocarcinoma.

Erlotinib is a highly specific and reversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), but resistance inevitably develops as the disease progresses. Erlotinib resistance and cancer stem cells (CSCs) are poor factors hindering the prognosis of patients with lung adenocarcinoma (LUAD). Although studies have shown that erlotinib resistance and CSCs can jointly promote cancer development, the mechanism is currently unclear. Here, we investigated the potential biomarker and molecular mechanism of erlotinib resistance and cancer stemness in LUAD. An erlotinib resistance model based on four genes was constructed from The Cancer Genome Atlas (TCGA), the GEO database, the Cancer Cell Line Encyclopedia (CCLE), and the Genomics of Drug Sensitivity in Cancer (GDSC). Through multiple bioinformatic analyses, was identified as a key gene for erlotinib resistance and stemness in LUAD. Further in vitro experiments demonstrated that maintains stemness and contributes to erlotinib resistance in LUAD. In summary, plays a vital role in stemness and erlotinib resistance in LUAD.