TRIP13 overexpression promotes gefitinib resistance in non‑small cell lung cancer via regulating autophagy and phosphorylation of the EGFR signaling pathway

• Published in: Oncology reports Vol. 49; no. 5; p. 1
• Main Authors: Xiao, Zhangxian, Li, Mingxi, Zhang, Xiaoqian, Rong, Xuezhu, Xu, Hongtao
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.05.2023; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Antineoplastic Agents - pharmacology; Antineoplastic Agents - therapeutic use; ATPases Associated with Diverse Cellular Activities - metabolism; Autophagy; Cancer therapies; Carcinoma, Non-Small-Cell Lung - drug therapy; Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - pathology; Care and treatment; Cell cycle; Cell Cycle Proteins - metabolism; Cell Line, Tumor; Chemotherapy; Computer software industry; Drug resistance; Drug Resistance, Neoplasm; Epidermal growth factor; ErbB Receptors - metabolism; Gefitinib; Gefitinib - pharmacology; Gefitinib - therapeutic use; Health aspects; Humans; Inhibitor drugs; Kinases; Lung cancer; Lung cancer, Non-small cell; Lung cancer, Small cell; Lung Neoplasms - drug therapy; Lung Neoplasms - genetics; Lung Neoplasms - pathology; Medical prognosis; Mutation; Phosphorylation; Plasmids; Proteins; Scientific equipment and supplies industry; Signal Transduction; Thyroid gland; Tumors; Tyrosine; United States; China; gefitinib resistance; autophagy; TRIP13; NSCLC; EGFR

Non‑small cell lung cancer (NSCLC) accounts for the majority of lung cancers and remains the most common cause of cancer‑related death. Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR‑TKIs) have been used as first‑line treatment for patients with NSCLC showing mutations. Unf...