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

Chen-Xing Hou; Li Wang; Man Cai; Ying Meng; Yu-Ting Tang; Qing-Hai Zhu; Wei Han; Nan-Nan Sun; Ben Ma; Yong Hu; Jin-Hai Ye

doi:10.1016/j.prp.2021.153620

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

Pathol Res Pract. 2021 Nov:227:153620. doi: 10.1016/j.prp.2021.153620. Epub 2021 Sep 16.

Authors

Chen-Xing Hou¹, Li Wang², Man Cai³, Ying Meng¹, Yu-Ting Tang¹, Qing-Hai Zhu¹, Wei Han¹, Nan-Nan Sun¹, Ben Ma⁴, Yong Hu⁴, Jin-Hai Ye⁵

Affiliations

¹ Jiangsu Key Laboratory of Oral Disease, Nanjing Medical University, Nanjing 210029, China; Depatment of Oral and Maxillofacial Surgery, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing 210029, China.
² Jiangsu Key Laboratory of Oral Disease, Nanjing Medical University, Nanjing 210029, China; Department of Stomatology, Wuxi Huishan District People's Hospital, Wuxi 214187, China.
³ Jiangsu Key Laboratory of Oral Disease, Nanjing Medical University, Nanjing 210029, China; Department of Stomatology, The Affiliated Suqian First People's Hospital of Nanjing Medical University, Suqian 223800, China.
⁴ Department of Stomatology, The Affiliated Suzhou Science & Technology Town Hospital of Nanjing Medical University, Suzhou 215153, China.
⁵ Jiangsu Key Laboratory of Oral Disease, Nanjing Medical University, Nanjing 210029, China; Depatment of Oral and Maxillofacial Surgery, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing 210029, China. Electronic address: yejinhai@njmu.edu.cn.

PMID: 34560416
DOI: 10.1016/j.prp.2021.153620

Abstract

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.

Keywords: PI3K/Akt; Proliferation; Salivary adenoid cystic carcinoma; Sphk1; Tumorigenesis.

MeSH terms

Apoptosis
Carcinoma, Adenoid Cystic / enzymology*
Carcinoma, Adenoid Cystic / genetics
Carcinoma, Adenoid Cystic / pathology
Cell Line, Tumor
Cell Movement
Cell Proliferation
Disease Progression
Epithelial-Mesenchymal Transition
Gene Expression Regulation, Neoplastic
Humans
Phosphatidylinositol 3-Kinase / metabolism*
Phosphorylation
Phosphotransferases (Alcohol Group Acceptor) / genetics
Phosphotransferases (Alcohol Group Acceptor) / metabolism*
Proto-Oncogene Proteins c-akt / metabolism*
Salivary Gland Neoplasms / enzymology*
Salivary Gland Neoplasms / genetics
Salivary Gland Neoplasms / pathology
Signal Transduction

Substances

Phosphotransferases (Alcohol Group Acceptor)
sphingosine kinase
Phosphatidylinositol 3-Kinase
Proto-Oncogene Proteins c-akt