Abstract
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, NCAPG2 was identified as a key gene for erlotinib resistance and stemness in LUAD. Further in vitro experiments demonstrated that NCAPG2 maintains stemness and contributes to erlotinib resistance in LUAD. In summary, NCAPG2 plays a vital role in stemness and erlotinib resistance in LUAD.
Funder
National Natural Science Foundation of China
Hunan Provincial Natural Science Foundation of China
Reference48 articles.
1. Lung Cancer Stem-like Cells and Drug Resistance;Pan;Chin. J. Lung Cancer,2022
2. Loss of KMT5C Promotes EGFR Inhibitor Resistance in NSCLC via LINC01510-Mediated Upregulation of MET
3. Erlotinib;Abdelgalil;Profiles Drug Subst. Excip. Relat. Methodol.,2020
4. Advances in the Research of Autophagy in EGFR-TKI Treatment and Resistance in Lung Cancer;Zhang;Chin. J. Lung Cancer,2016
5. First-line treatment of advanced epidermal growth factor receptor (EGFR) mutation positive non-squamous non-small cell lung cancer
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