Xiao Xin, Xu Juan, Sheng Xiaoan, Wang Chao, Dong Juanjuan, Shi Xianfeng
Department of Oncology, Chaohu Hospital Affiliated to Anhui Medical University, Chaohu, Anhui 231500, P.R. China.
Exp Ther Med. 2023 Feb 10;25(3):131. doi: 10.3892/etm.2023.11830. eCollection 2023 Mar.
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.
烟草中的尼古丁具有致癌性,是肺癌的一个众所周知的风险因素。然而,烟草中的尼古丁是否能诱导肺癌产生耐药性尚不清楚。本研究的目的是确定在肺癌吸烟者和非吸烟者中差异表达的长链非编码RNA(lncRNA)对肿瘤坏死因子相关凋亡诱导配体(TRAIL)的耐药性。结果表明,尼古丁上调了小核仁RNA宿主基因5(SNHG5),并显著降低了裂解的半胱天冬酶-3的水平。本研究发现,细胞质lncRNA SNHG5的过表达与肺癌中的TRAIL耐药性相关,并且SNHG5可以与X连锁凋亡抑制蛋白相互作用以促进TRAIL耐药性。因此,尼古丁通过SNHG5/X连锁凋亡抑制蛋白促进了肺癌中的TRAIL耐药性。