CHST15在食管癌中通過多種途徑促進TE - 1細胞的增殖

2019年5月，中國醫學科學院北京協和醫學院腫瘤醫院國家腫瘤中心/國家腫瘤臨床研究中心放射腫瘤科；北京環星腫瘤醫院放療科；中國醫學科學院；北京協和醫學院附屬腫瘤醫院；深圳醫院國家腫瘤中心/國家腫瘤臨床研究中心放射腫瘤科 (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老師研究團隊在《ONCOLOGY》上發表論文：

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

“CHST15在食管癌中通過多種途徑促進TE - 1細胞的增殖”

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：

食管鱗狀細胞癌(ESCC)是一種常見的食管癌，在世界范圍內普遍存在。由于化療耐藥的發生，了解其形成機制和尋找更有效的治療策略至關重要。本研究的目的是確定碳水化合物硫轉移酶15 (CHST15)在ESCC中的功能相關性和治療潛力。在不同ESCC細胞系中測量CHST15水平，并使用組織芯片免疫組織化學方法評估ESCC組織中的CHST15水平。采用TE-1細胞進行細胞生長和凋亡實驗、3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑實驗和克隆生成實驗，并利用lentit - shchst15病毒構建體研究CHST15在細胞增殖和凋亡中的作用。通過mRNA芯片分析確定CHST15調控TE-1細胞增殖和凋亡的潛在機制。結果表明，CHST15基因敲低可抑制TE-1細胞的生長和增殖，但可誘導細胞凋亡。與正常食管組織相比，ESCC組織中CHST15的檢出率更高。芯片數據分析表明，CHST15敲低細胞的細胞增殖抑制和細胞凋亡激活可能分別由CHST15/ILKAP/CCND1和CHST15/RABL6/PMAIP1信號軸改變引起。

該論文中ESCC細胞系TE-1、Eca-109和EC9706細胞的體外培養是使用Ausbian特級胎牛血清完成的。欲了解或購買Ausbian特級胎牛血清可以聯系北京締一生物400-166-8600.