Overexpression of OCT4 is associated with gefitinib resistance in non-small cell lung cancer.

Abstract

Epidermal growth factor receptor (EGFR)-targeted tyrosine kinase inhibitors (TKIs) have emerged as first-line drugs for non-small cell lung cancers (NSCLCs). However, the resistance to TKIs represents the key limitation for their therapeutic efficacy. We found that the difference of OCT4 expression between NSCLC and the adjacent non-tumourous tissues was statistically significant. Knockdown of OCT4 in NSCLC cells could decrease cell proliferation, and potentiate apoptosis induced by gefitinib, suggesting OCT4 may contribute to gefitinib resistance in NSCLC.

• Authors: Bin Li, Zhouhong Yao, Yunyan Wan, Dianjie Lin
• Journal: Oncotarget (Oncotarget) Vol. 7 Issue 47 Pg. 77342-77347 (Nov 22 2016) ISSN: 1949-2553 [Electronic] United States
• PMID: 27816965 (Publication Type: Journal Article)

Chemical References

• Antineoplastic Agents
• Octamer Transcription Factor-3
• POU5F1 protein, human
• Protein Kinase Inhibitors
• Quinazolines
• RNA, Small Interfering
• ErbB Receptors
• Gefitinib

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Carcinoma, Non-Small-Cell Lung (drug therapy, genetics, metabolism)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Drug Resistance, Neoplasm (genetics)
• ErbB Receptors (metabolism)
• Gefitinib
• Gene Expression
• Gene Expression Regulation, Neoplastic
• Humans
• Lung Neoplasms (drug therapy, genetics, metabolism)
• Mutation
• Octamer Transcription Factor-3 (genetics)
• Protein Kinase Inhibitors (pharmacology)
• Quinazolines (pharmacology)
• RNA Interference
• RNA, Small Interfering (genetics)