Zhou Huan, Chen Guang
Department of Medical Oncology, Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Department of Traumatic Orthopedics, Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Afr Health Sci. 2024 Sep;24(3):173-179. doi: 10.4314/ahs.v24i3.21.
To analyse how Semaphorin 6D (SEMA6D) expression and extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signal pathways are activated and how they influence gastric cancer proliferation, migration, and invasion.
SEMA6D expression was knocked down in human gastric cancer cells using RNA interference technology. In vitro assays were used to analyse how SEMA6D knockdown affects clone formation, migration, and invasion. ERK and PI3K/AKT/mTOR signaling pathway related proteins were detected by immunoblotting.
In the si-NC group, Sema6D protein levels were higher than those in the si-1 and si-2 groups after knockdown of Sema6D, while in the si-1 group, Sema6D protein levels were higher than those in the si-2 group (P<0.05). P-PI3K, ERK/p-ERK, AKT/p-AKT, and mTOR/p-mTOR levels in the si-NC group were significantly higher than those in the si-1 and si-2 groups after knockdown of Sema6D (P < 0.05). It was found that scratch healing rate of SGC-7901 cells in si-NC group was higher than that in si-1 and si-2 groups, and the difference was statistically significant (P < 0.05).
SEMA6D expression level can affect the biological behavior of gastric cancer cells.
分析信号素6D（SEMA6D）的表达以及细胞外信号调节激酶（ERK）、磷脂酰肌醇3激酶/蛋白激酶B/雷帕霉素哺乳动物靶蛋白（PI3K/AKT/mTOR）信号通路是如何被激活的，以及它们如何影响胃癌的增殖、迁移和侵袭。
使用RNA干扰技术在人胃癌细胞中敲低SEMA6D的表达。采用体外试验分析SEMA6D敲低对克隆形成、迁移和侵袭的影响。通过免疫印迹检测ERK和PI3K/AKT/mTOR信号通路相关蛋白。
在si-NC组中，敲低Sema6D后，Sema6D蛋白水平高于si-1组和si-2组，而在si-1组中，Sema6D蛋白水平高于si-2组（P<0.05）。敲低Sema6D后，si-NC组中P-PI3K、ERK/p-ERK、AKT/p-AKT和mTOR/p-mTOR水平显著高于si-1组和si-2组（P<0.05）。发现si-NC组中SGC-7901细胞的划痕愈合率高于si-1组和si-2组，差异具有统计学意义（P<0.05）。
SEMA6D表达水平可影响胃癌细胞的生物学行为。
