Xiaobo Yu, Qiang Lin, Xiong Qin, Zheng Ruan, Jianhua Zhou, Zhifeng Lin, Yijiang Su, Zheng Jian
Department of Thoracic Surgery, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai 200080, China.
Department of Thoracic Surgery, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai 200080, China.
Gene. 2016 Jan 15;576(1 Pt 2):339-46. doi: 10.1016/j.gene.2015.10.072. Epub 2015 Nov 11.
Serum and glucocorticoid kinase 1 (SGK1) has been reported to be up-regulated in non-small cell lung cancer (NSCLC). However, its functions in NSCLC remained unclear. Here, SGK1 was found to be up-regulated in NSCLC samples. Over-expression of SGK1 promoted the growth and migration of NSCLC cells, while down-regulation of SGK1 inhibited the growth, migration and metastasis of NSCLC cells. SGK1 promoted the phosphorylation of GSK3 beta and the accumulation of beta-catenin, up-regulation of the target genes downstream of beta-catenin/TCF signaling, and activating the transcriptional activity of beta-catenin/TCF complex. Collectively, SGK1 might promote the progression of NSCLC through activating beta-catenin/TCF signaling.
血清和糖皮质激素激酶1（SGK1）在非小细胞肺癌（NSCLC）中被报道上调。然而，其在NSCLC中的功能仍不清楚。在此，发现SGK1在NSCLC样本中上调。SGK1的过表达促进了NSCLC细胞的生长和迁移，而SGK1的下调则抑制了NSCLC细胞的生长、迁移和转移。SGK1促进糖原合成酶激酶3β（GSK3β）的磷酸化和β-连环蛋白的积累，上调β-连环蛋白/TCF信号下游的靶基因，并激活β-连环蛋白/TCF复合物的转录活性。总的来说，SGK1可能通过激活β-连环蛋白/TCF信号促进NSCLC的进展。
