Sphk1 promotes salivary adenoid cystic carcinoma progression via PI3K/ Akt signaling

被引：12
|
作者：
Hou, Chen-xing [1 ,2 ]
Wang, Li [1 ,4 ]
Cai, Man [1 ,5 ]
Meng, Ying [1 ,2 ]
Tang, Yu-ting [1 ,2 ]
Zhu, Qing-hai [1 ,2 ]
Han, Wei [1 ,2 ]
Sun, Nan-nan [1 ,2 ]
Ma, Ben [3 ]
Hu, Yong [3 ]
Ye, Jin-hai [1 ,2 ]
机构：
[1] Nanjing Med Univ, Jiangsu Key Lab Oral Dis, Nanjing 210029, Peoples R China
[2] Nanjing Med Univ, Affiliated Stomatol Hosp, Dept Oral & Maxillofacial Surg, Hanzhong Rd 136, Nanjing 210029, Peoples R China
[3] Nanjing Med Univ, Dept Stomatol, Affiliated Suzhou Sci & Technol Town Hosp, Suzhou 215153, Peoples R China
[4] Wuxi Huishan Dist Peoples Hosp, Dept Stomatol, Wuxi 214187, Jiangsu, Peoples R China
[5] Nanjing Med Univ, Affiliated Suqian First Peoples Hosp, Dept Stomatol, Suqian 223800, Peoples R China
来源：
PATHOLOGY RESEARCH AND PRACTICE | 2021年 / 227卷
关键词：
Salivary adenoid cystic carcinoma; Sphk1; PI3K; Akt; Tumorigenesis; Proliferation; EPITHELIAL-MESENCHYMAL TRANSITION; CANCER; PATHWAY; KINASE; NECK; HEAD; EMT;
D O I：
10.1016/j.prp.2021.153620
中图分类号：
R36 [病理学];
学科分类号：
100104 ;
摘要：
The progression of salivary adenoid cystic carcinoma (SACC) is closely related to abnormal gene expression. Herein, the role of Sphk1 in SACC was explored. Sphk1 was overexpressed in SACC tissues. In SACC cell lines, Sphk1 induced cell proliferation, inhibited apoptosis, and promoted cell migration. Moreover, Sphk1 overexpression induced up-regulation of the PI3K protein level and AKT phosphorylation level. Rescue assays further showed that activation of the Sphk1 /PI3K/Akt pathway affected various biological functions of SACC cells. Together, these findings suggested that Sphk1 promotes salivary tumorigenesis by activating the PI3K/ Akt pathway, which may provide novel intervention targets for SACC treatment.
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页数：6
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