CHST15 promotes the proliferation of TE-1 cells via multiple pathways in esophageal cancer
CHST15 promotes the proliferation of TE-1 cells via multiple pathways in esophageal cancer
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DOI：
10.3892/or.2019.7395
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发表时间：
2020-01-01
期刊：
影响因子：
4.2
通讯作者：
Wang, Luhua
中科院分区：
文献类型：
--
作者：
Wang, Xin;Cheng, Guowei;Wang, Luhua
食管鳞状细胞癌（ESCC）是一种常见的食管癌类型，在世界范围内流行。了解其形成的机制和寻找更有效的治疗策略是至关重要的，由于化疗药物耐药性的发生。本研究的目的是确定碳水化合物磺基转移酶15（CHST 15）在ESCC中的功能相关性和治疗潜力。在不同的ESCC细胞系中测量CHST 15水平，并使用组织芯片免疫组织化学在ESCC组织中进行评估。使用TE-1细胞进行细胞生长和凋亡测定、3-（4，5-二甲基噻唑-2-基）-2，5-二苯基溴化四唑测定和克隆形成测定，并使用慢-shCHST 15病毒构建体研究CHST 15在细胞增殖和凋亡中的功能。mRNA微阵列分析，以确定CHST 15的调节TE-1细胞增殖和凋亡的潜在机制。结果表明，CHST 15基因的敲低抑制TE-1细胞的生长和增殖，但诱导细胞凋亡。CHST 15在食管鳞癌组织中的表达高于正常食管组织。芯片数据分析表明，CHST 15敲低细胞中细胞增殖的抑制和细胞凋亡的激活可能分别由CHST 15/ILKAP/CCND 1和CHST 15/RABL 6/PMAIP 1信号轴的改变引起。
Esophageal squamous cell carcinoma (ESCC) is a common type of esophageal cancer and is prevalent worldwide. Understanding the mechanisms underlying its formation and the search for more effective therapeutic strategies are critical due to the occurrence of chemotherapeutic drug resistance. The aim of the present study was to determine the functional relevance and therapeutic potential of carbohydrate sulfotransferase 15 (CHST15) in ESCC. CHST15 levels were measured in different ESCC cell lines and evaluated in ESCC tissues using tissue chip immunohistochemistry. Cell growth and apoptosis assays, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, and clonogenic assays were conducted using TE-1 cells and lenti-shCHST15 virus constructs were used to investigate the function of CHST15 in cell proliferation and apoptosis. mRNA microarray analysis was performed to determine the underlying mechanism of CHST15 regulation in TE-1 cell proliferation and apoptosis. The results showed that knockdown of CHST15 inhibited TE-1 cell growth and proliferation, but induced cell apoptosis. CHST15 was more frequently detected in ESCC tissue compared with that in normal esophageal tissue. Microarray data analysis indicated that the inhibition of cell proliferation and activation of cell apoptosis in CHST15-knockdown cells may be caused by altered CHST15/ILKAP/CCND1 and CHST15/RABL6/PMAIP1 signaling axes, respectively.