CHST15在食管癌中通过多种途径促进TE - 1细胞的增殖

2019年5月，中国医学科学院北京协和医学院肿瘤医院国家肿瘤中心/国家肿瘤临床研究中心放射肿瘤科；北京环星肿瘤医院放疗科；中国医学科学院；北京协和医学院附属肿瘤医院；深圳医院国家肿瘤中心/国家肿瘤临床研究中心放射肿瘤科 (Department of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021;   Department of Radiotherapy, Huanxing Tumor Hospital, Beijing 100023；Department of Radiation Oncology,National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital and Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, Guangdong 518116, P.R. China) XIN WANG老师研究团队在《ONCOLOGY》上发表论文：

“CHST15 promotes the proliferation of TE‑1 cells via multiple pathways in esophageal cancer”

“CHST15在食管癌中通过多种途径促进TE - 1细胞的增殖”

Abstract：

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(4,5dimethylthiazol2yl)2,5diphenyltetrazolium bromide assays, and clonogenic assays were conducted using TE1 cells and lentishCHST15 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 TE1 cell proliferation and apoptosis. The results showed that knockdown of CHST15 inhibited TE1 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 CHST15knockdown cells may be caused by altered CHST15/ILKAP/CCND1 and CHST15/RABL6/PMAIP1 signaling axes, respectively.

摘要：

食管鳞状细胞癌(ESCC)是一种常见的食管癌，在世界范围内普遍存在。由于化疗耐药的发生，了解其形成机制和寻找更有效的治疗策略至关重要。本研究的目的是确定碳水化合物硫转移酶15 (CHST15)在ESCC中的功能相关性和治疗潜力。在不同ESCC细胞系中测量CHST15水平，并使用组织芯片免疫组织化学方法评估ESCC组织中的CHST15水平。采用TE-1细胞进行细胞生长和凋亡实验、3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑实验和克隆生成实验，并利用lentit - shchst15病毒构建体研究CHST15在细胞增殖和凋亡中的作用。通过mRNA芯片分析确定CHST15调控TE-1细胞增殖和凋亡的潜在机制。结果表明，CHST15基因敲低可抑制TE-1细胞的生长和增殖，但可诱导细胞凋亡。与正常食管组织相比，ESCC组织中CHST15的检出率更高。芯片数据分析表明，CHST15敲低细胞的细胞增殖抑制和细胞凋亡激活可能分别由CHST15/ILKAP/CCND1和CHST15/RABL6/PMAIP1信号轴改变引起。

该论文中ESCC细胞系TE-1、Eca-109和EC9706细胞的体外培养是使用Ausbian特级胎牛血清完成的。欲了解或购买Ausbian特级胎牛血清可以联系北京缔一生物400-166-8600.