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

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.

Automated summary

Sphk1 is overexpressed in salivary adenoid cystic carcinoma (SACC), promoting tumorigenesis by activating the PI3K/Akt pathway. This finding provides novel intervention targets for SACC treatment.