鞘氨醇激酶 1 通过 PI3K/Akt 信号通路促进唾液腺腺样囊性癌的进展。
Sphk1 promotes salivary adenoid cystic carcinoma progression via PI3K/Akt signaling.
机构信息
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.
Jiangsu Key Laboratory of Oral Disease, Nanjing Medical University, Nanjing 210029, China; Department of Stomatology, Wuxi Huishan District People's Hospital, Wuxi 214187, China.
出版信息
Pathol Res Pract. 2021 Nov;227:153620. doi: 10.1016/j.prp.2021.153620. Epub 2021 Sep 16.
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.
唾液腺腺样囊性癌（SACC）的进展与异常基因表达密切相关。本文探讨了 Sphk1 在 SACC 中的作用。Sphk1 在 SACC 组织中过表达。在 SACC 细胞系中，Sphk1 诱导细胞增殖，抑制细胞凋亡，促进细胞迁移。此外，Sphk1 过表达诱导 PI3K 蛋白水平和 AKT 磷酸化水平上调。挽救实验进一步表明，Sphk1/PI3K/Akt 通路的激活影响 SACC 细胞的各种生物学功能。综上所述，这些发现表明 Sphk1 通过激活 PI3K/Akt 通路促进唾液肿瘤发生，这可能为 SACC 的治疗提供新的干预靶点。
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