Department of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, China.
Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, China.
J Cancer Res Clin Oncol. 2024 Oct 12;150(10):456. doi: 10.1007/s00432-024-05938-5.
The SCY1-like (SCYL) family has been reported to be closely related to cancer metastasis, but it has not been reported in gastric cancer (GC), and its specific mechanism is not clear.
We utilized databases like Deepmap, TCGA, and GEO to identify SCYL1's role in GC. Clinical samples were analyzed for SCYL1 expression and its correlation with patient prognosis. In vitro and in vivo experiments were conducted to assess SCYL1's function in GC cell migration, invasion, and autophagy.
SCYL1 showed an increased expression in GC tissues, which correlated with a negative prognosis. In vitro experiments demonstrated that SCYL1 promotes GC cell migration and invasion and inhibits autophagy. GSEA indicated an inverse relationship between SCYL1 and autophagy, while a direct relationship was observed with the mTORC1 signaling pathway. Knockdown of SCYL1 enhanced autophagy, while activation of mTORC1 reversed this effect.
SCYL1 is a significant contributor to GC progression, promoting metastasis by activating the mTORC1 signaling pathway and inhibiting autophagy. These findings suggest SCYL1 as a potential therapeutic target for GC treatment.
SCY1 样（SCYL）家族与癌症转移密切相关，但尚未在胃癌（GC）中报道，其具体机制尚不清楚。
我们利用 Deepmap、TCGA 和 GEO 等数据库来确定 SCYL1 在 GC 中的作用。分析临床样本中 SCYL1 的表达及其与患者预后的相关性。进行体外和体内实验以评估 SCYL1 在 GC 细胞迁移、侵袭和自噬中的功能。
SCYL1 在 GC 组织中表达增加，与预后不良相关。体外实验表明，SCYL1 促进 GC 细胞迁移和侵袭，抑制自噬。GSEA 表明 SCYL1 与自噬呈负相关，而与 mTORC1 信号通路呈正相关。SCYL1 的敲低增强了自噬，而 mTORC1 的激活则逆转了这种作用。
SCYL1 是 GC 进展的重要贡献者，通过激活 mTORC1 信号通路和抑制自噬促进转移。这些发现表明 SCYL1 可能成为 GC 治疗的潜在治疗靶点。
