报道称，鞘氨醇激酶-2（SphK2）是鞘脂信号转导的主要成分，是一种创新的治疗癌症的候选药物。本研究旨在调查SphK2在通过诱导细胞凋亡和靶向C-FLIPS、MCL-1和survivin表达，增加HT-29结肠直肠癌细胞对紫杉醇的敏感性中发挥的作用。细胞分别被转染了针对SphK2、PTX或SphK2激动剂的siRNA。通过MTT测定细胞增殖，通过尝试蓝染色和ELISA评估细胞凋亡。采用qRT-PCR和Western印迹确定SphK2、C-FLIPS、MCL-1和survivin表达。结果表明，SphK2 siRNA可以增加由PTX诱导的细胞死亡。SphK2激动剂可以消除siRNA对细胞存活的影响。我们发现，siRNA转染会引起C-FLIPS、MCL-1和survivin的过度表达，不管是单独使用还是在紫杉醇处理的细胞中，都会导致细胞凋亡的增加。研究结果表明，抑制SphK2可能是增强结肠癌细胞对紫杉醇敏感性的一种有效方法，能够通过诱导细胞凋亡发挥这一作用。本文受版权保护。版权所有，不得转载。

The sphingosine kinase-2 (SphK2), a main component of sphingolipid signal transduction, is reported as an innovative therapeutic candidate for cancer treatment. This study was conducted to investigate the involvement of SphK2 in increasing HT-29 colorectal cancer cells sensitivity to paclitaxel via inducing apoptosis and targeting c-FLIPS, MCL-1 and survivin expressions. Cells were transfected with siRNA against SphK2, PTX or SphK2 activator. Proliferation and apoptosis were evaluated by MTT assay, and trypan blue staining and ELISA, respectively. SphK2, c-FLIPS, MCL-1 and survivin expression were determined by qRT-PCR and western blotting. SphK2 siRNA increased cell death induced PTX. SphK2 agonist abolished silencing impact on cell survival. We found overexpression of C-FLIPS, MCL-1 and survivin by siRNA transfection either alone or in paclitaxel treated cells, as well as elevation in cell apoptosis. Our results showed that SphK2 suppression may be an effective important modality to enhance cell sensitivity to paclitaxel via the induction of apoptosis in colorectal cancers.This article is protected by copyright. All rights reserved.