Sphk1 promotes salivary adenoid cystic carcinoma progression via PI3K/Akt signaling.
Apoptosis
Carcinoma, Adenoid Cystic
/ enzymology
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
Proto-Oncogene Proteins c-akt
/ metabolism
Salivary Gland Neoplasms
/ enzymology
Signal Transduction
PI3K/Akt
Proliferation
Salivary adenoid cystic carcinoma
Sphk1
Tumorigenesis
Journal
Pathology, research and practice
ISSN: 1618-0631
Titre abrégé: Pathol Res Pract
Pays: Germany
ID NLM: 7806109
Informations de publication
Date de publication:
Nov 2021
Nov 2021
Historique:
received:
27
07
2021
revised:
06
09
2021
accepted:
10
09
2021
pubmed:
25
9
2021
medline:
3
3
2022
entrez:
24
9
2021
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 34560416
pii: S0344-0338(21)00281-8
doi: 10.1016/j.prp.2021.153620
pii:
doi:
Substances chimiques
Phosphotransferases (Alcohol Group Acceptor)
EC 2.7.1.-
sphingosine kinase
EC 2.7.1.-
Phosphatidylinositol 3-Kinase
EC 2.7.1.137
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
153620Informations de copyright
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