Abstract
Atractyloside is a traditional Chinese medicine used to treat nasal congestion, and allergic rhinitis; however, its effects on cancer are unknown. Non-small cell lung cancer (NSCLC) is associated with high mortality rates worldwide, and relapse due to epidermal growth factor receptor mutations is a problem in clinical therapy. Therefore, novel biomarkers are required for the diagnosis and treatment of NSCLC. Brother of the regulator of imprinted sites (BORIS; also known as CTCFL) is a potential therapeutic target in NSCLC. BORIS promotes cisplatin resistance and it has been suggested that it may account for multidrug resistance. The present study examined BORIS expression in tyrosine kinase inhibitor (TKI)-resistant NSCLC cells. Subsequently, small interfering RNA was used to knock down BORIS expression, and the effects of this knockdown were assessed on TKI-resistant NSCLC cell viability. The present study also investigated the effect of atractyloside on the proliferation of NSCLC cells using MTT assay. The results of the present study indicated that the inhibition of BORIS or its related downstream pathways may have potential for the treatment of TKI-resistant NSCLC. In addition, atractyloside mimicked BORIS knockdown, regulated its downstream genes and inhibited the proliferation of TKI-resistant NSCLC cells. In conclusion, the findings of the present study supported the potential application of atractyloside in TKI-resistant NSCLC therapy.