Department of General Surgery, The Second Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China.
Department of GI Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Hum Exp Toxicol. 2021 Oct;40(10):1646-1655. doi: 10.1177/09603271211006168. Epub 2021 Apr 7.
Visfatin acts as an oncogenic factor in numerous tumors through a variety of cellular processes. Visfatin has been revealed to promote cell migration and invasion in gastric cancer (GC). Snai1 is a well-known regulator of EMT process in cancers. However, the relationship between visfatin and snai1 in GC remains unclear. The current study aimed to explore the role of visfatin in GC.
The RT-qPCR and western blot analysis were used to measure RNA and protein levels, respectively. The cell migration and invasion were tested by Trans-well assays and western blot analysis.
Visfatin showed upregulation in GC cells. Additionally, Visfatin with increasing concentration facilitated epithelial-mesenchymal transition (EMT) process by increasing E-cadherin and reducing N-cadherin and Vimentin protein levels in GC cells. Moreover, endogenous overexpression and knockdown of visfatin promoted and inhibited migratory and invasive abilities of GC cells, respectively. Then, we found that snai1 protein level was positively regulated by visfatin in GC cells. In addition, visfatin activated the NF-κB signaling to modulate snai1 protein expression. Furthermore, the silencing of snai1 counteracted the promotive impact of visfatin on cell migration, invasion and EMT process in GC.
Visfatin facilitates cell migration, invasion and EMT process by targeting snai1 via the NF-κB signaling, which provides a potential insight for the treatment of GC.
脂联素在多种肿瘤中通过多种细胞过程发挥致癌因子的作用。脂联素已被证明可促进胃癌（GC）中的细胞迁移和侵袭。Snai1 是癌症中 EMT 过程的已知调节剂。然而，脂联素和 Snai1 在 GC 中的关系尚不清楚。本研究旨在探讨脂联素在 GC 中的作用。
使用 RT-qPCR 和 Western blot 分析分别测量 RNA 和蛋白质水平。通过 Trans-well 测定和 Western blot 分析测试细胞迁移和侵袭。
脂联素在 GC 细胞中上调。此外，脂联素浓度增加通过增加 GC 细胞中 E-钙粘蛋白并减少 N-钙粘蛋白和波形蛋白蛋白水平促进上皮-间充质转化（EMT）过程。此外，内源性过表达和敲低脂联素分别促进和抑制 GC 细胞的迁移和侵袭能力。然后，我们发现 snai1 蛋白水平在 GC 细胞中被脂联素正向调节。此外，脂联素激活 NF-κB 信号通路来调节 snai1 蛋白表达。此外，snai1 的沉默抵消了脂联素对 GC 细胞迁移、侵袭和 EMT 过程的促进作用。
脂联素通过 NF-κB 信号通路靶向 snai1 促进细胞迁移、侵袭和 EMT 过程，为 GC 的治疗提供了潜在的见解。
