Department of Orthopedics, Second Affiliated Hospital of Nantong University, Nantong, 226000, Jiangsu, People's Republic of China.
School of Medicine, Nantong University, Nantong, 226000, Jiangsu, People's Republic of China.
J Orthop Surg Res. 2020 Apr 25;15(1):162. doi: 10.1186/s13018-020-01679-6.
This article reports the effects of proenkephalin (PENK) on osteosarcoma (OS) cell migration.
A Gene Expression Omnibus (GEO) dataset was used to identify differentially expressed genes (DEGs) in OS tumor samples and normal human osteoblasts. Tumor tissue and adjacent normal tissue were collected from 40 OS patients. MG63 cells were transfected with si-PENK. Transwell migration assays and wound healing assays were performed to compare the effect of PENK on migration. Moreover, LY294002 was used to identify the potential mechanism. Gene expression was examined via qRT-PCR and Western blotting.
Bioinformatic analysis revealed that PENK was downregulated in OS tumor samples compared with normal human osteoblasts. Moreover, PENK was identified as the hub gene of the DEGs. The PI3K/Akt signaling pathway was significantly enriched in the DEGs. Moreover, PENK was downregulated in OS and MG63 cells compared with the corresponding control cells. Silencing PENK promoted MG63 cell migration; however, treatment with LY294002 partially attenuated PENK silencing-induced OS cell migration.
PENK inhibits OS cell migration by activating the PI3K/Akt signaling pathway.
本文报道了脑啡肽原(PENK)对骨肉瘤(OS)细胞迁移的影响。
使用基因表达综合数据库(GEO)数据集鉴定 OS 肿瘤样本和正常人类成骨细胞中的差异表达基因(DEGs)。收集 40 例 OS 患者的肿瘤组织和相邻正常组织。将 si-PENK 转染至 MG63 细胞。通过 Transwell 迁移实验和划痕愈合实验比较 PENK 对迁移的影响。此外,使用 LY294002 鉴定潜在机制。通过 qRT-PCR 和 Western blot 检测基因表达。
生物信息学分析显示,与正常人类成骨细胞相比,OS 肿瘤样本中 PENK 下调。此外,PENK 被鉴定为 DEGs 的枢纽基因。PI3K/Akt 信号通路在 DEGs 中显著富集。此外,与相应对照细胞相比,OS 和 MG63 细胞中 PENK 下调。沉默 PENK 促进 MG63 细胞迁移;然而,用 LY294002 处理可部分减弱 PENK 沉默诱导的 OS 细胞迁移。
PENK 通过激活 PI3K/Akt 信号通路抑制 OS 细胞迁移。