Liu Wei, Ning Jinfeng, Li Chunhong, Hu Jing, Meng Qingwei, Lu Hailing, Cai Li
The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Haping Road 150, Harbin, 150040, People's Republic of China.
The Thoracic Surgery Department, Harbin Medical University Cancer Hospital, Harbin, 150040, People's Republic of China.
Tumour Biol. 2016 May;37(5):6331-6. doi: 10.1007/s13277-015-4480-1. Epub 2015 Dec 1.
Lung cancer is the major cause of cancer-related death worldwide, and 80 % of them are non-small cell lung cancer (NSCLC) cases. Recent studies have shown that sphingosine kinase 2 (SphK2) could promote tumor progression; however, whether SphK2 could affect the chemoresistance of NSCLC to chemotherapy remains unclear. To determine whether SphK2 serves as a potential therapeutic target of NSCLC, we utilized small interference RNA (siRNA) to knock down SphK2 expression in human NSCLC cells and analyzed their phenotypic changes. The data demonstrated that knockdown of SphK2 led to decreased proliferation and enhanced chemosensitivity and apoptosis to gefitinib in NSCLC cells. In this study, we describe the findings that overexpression of SphK2 promotes chemoresistance in NSCLC cells. Inhibition of SphK2 might be considered as a strategy in NSCLC treatment with gefitinib.
肺癌是全球癌症相关死亡的主要原因,其中80%为非小细胞肺癌(NSCLC)病例。最近的研究表明,鞘氨醇激酶2(SphK2)可促进肿瘤进展;然而,SphK2是否会影响NSCLC对化疗的耐药性仍不清楚。为了确定SphK2是否是NSCLC的潜在治疗靶点,我们利用小干扰RNA(siRNA)敲低人NSCLC细胞中SphK2的表达,并分析其表型变化。数据表明,敲低SphK2可导致NSCLC细胞增殖减少,对吉非替尼的化疗敏感性和凋亡增强。在本研究中,我们描述了SphK2过表达促进NSCLC细胞化疗耐药性的研究结果。抑制SphK2可能被视为NSCLC吉非替尼治疗的一种策略。