Tobacco nicotine promotes TRAIL resistance in lung cancer through SNHG5

Tobacco nicotine use is carcinogenic and a well-known risk factor for lung cancer. However, whether tobacco nicotine can induce drug resistance in lung cancer is not clear. The objective of the present study was to identify the TNF-related apoptosis-inducing ligand (TRAIL) resistance of long noncoding RNAs (lncRNAs) that are differentially expressed in smokers and nonsmokers with lung cancer. The results suggested that the nicotine upregulated small nucleolar RNA host gene 5 (SNHG5) and markedly decreased the levels of cleaved caspase-3. The present study found that cytoplasm lncRNA SNHG5 overexpression was associated with TRAIL resistance in lung cancer and that SNHG5 can interact with X-linked inhibitor of apoptosis protein to promote TRAIL resistance. Therefore, nicotine promoted TRAIL resistance in lung cancer through SNHG5/X-linked inhibitor of apoptosis protein.

Automated summary

Tobacco nicotine use is a known risk factor for lung cancer, but its role in inducing drug resistance is unclear. This study found that nicotine upregulated the expression of SNHG5 and decreased caspase-3 levels, leading to TRAIL resistance in smokers with lung cancer. SNHG5 was found to interact with X-linked inhibitor of apoptosis protein, promoting TRAIL resistance. These findings demonstrate that nicotine promotes TRAIL resistance through the SNHG5/X-linked inhibitor of apoptosis protein pathway in lung cancer.