INCAPG2/I Maintains Cancer Stemness and Promotes Erlotinib Resistance in Lung Adenocarcinoma

• Published in: Cancers Vol. 14; no. 18
• Main Authors: Jiang, Shiyao, Huang, Jingjing, He, Hua, Liu, Yueying, Liang, Lu, Sun, Xiaoyan, Li, Yi, Cong, Li, Qing, Bei, Jiang, Yiqun
• Format: Journal Article
• Language: English
• Published: MDPI AG 01.09.2022
• Subjects: Adenocarcinoma; Dosage and administration; Drug resistance; Drug therapy; Erlotinib; Genetic aspects; Health aspects; Lung cancer; Stem cells; China
• ISSN: 2072-6694; 2072-6694
• DOI: 10.3390/cancers14184395

This study investigated the relationship between erlotinib resistance and stemness in lung adenocarcinoma. NCAPG2 was identified as an erlotinib resistance gene and maintained the stemness of 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, 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.