Yi Yun, Liao Bing, Zheng Ziwen, Yang Xiaorong, Yang Yunsheng, Zhou Yanfang, Tan Buzhen, Yang Xinfeng
Department of Gynecological Oncology, Cancer Hospital Affiliated to Nanchang University, Nanchang, Jiangxi 330029, P.R. China.
Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330000, P.R. China.
Exp Ther Med. 2021 Apr;21(4):372. doi: 10.3892/etm.2021.9803. Epub 2021 Feb 19.
DEC1 has been reported to regulate the expression of multiple target genes, participate in cell differentiation, apoptosis, aging and the development and progression of numerous tumors, but the detailed effects and possible mechanisms of DEC1 in ovarian cancer (OC) remain unknown. The present study aimed to investigate the expression and mechanism of function of DEC1 in OC. The present results demonstrated that DEC1 was highly expressed in OC tissues and cell lines using reverse transcription-quantitative PCR, western blotting and immunohistochemistry, and high expression of DEC1 was negatively associated with the prognosis of patients with OC. In addition, knockdown of DEC1 significantly inhibited proliferation in SKOV3 and OVCAR3 cells compared with control. DEC1 knockdown also induced apoptosis and increased the expression of apoptosis-related proteins in OC cells. The results suggested that knockdown of DEC1 inhibited OC cell migration and invasion via regulation of epithelial-mesenchymal transition-related protein. It was also found that DEC1 knockdown significantly inhibited the Wnt/β-catenin pathway. Collectively, the current results indicated that knockdown of DEC1 inhibited proliferation, migration and invasion, and induced apoptosis in OC cells via modulating the Wnt/β-catenin signaling pathway. Thus, DEC1 may participate in malignant progression of OC, and may be a target for treatment and diagnosis of OC.
据报道，DEC1可调节多个靶基因的表达，参与细胞分化、凋亡、衰老以及众多肿瘤的发生和发展，但DEC1在卵巢癌（OC）中的具体作用及可能机制仍不清楚。本研究旨在探讨DEC1在OC中的表达及其功能机制。本研究结果通过逆转录定量PCR、蛋白质印迹法和免疫组织化学法表明，DEC1在OC组织和细胞系中高表达，且DEC1的高表达与OC患者的预后呈负相关。此外，与对照组相比，敲低DEC1可显著抑制SKOV3和OVCAR3细胞的增殖。敲低DEC1还可诱导OC细胞凋亡并增加凋亡相关蛋白的表达。结果表明，敲低DEC1通过调节上皮-间质转化相关蛋白抑制OC细胞的迁移和侵袭。还发现敲低DEC1可显著抑制Wnt/β-连环蛋白信号通路。总体而言，目前的结果表明，敲低DEC1通过调节Wnt/β-连环蛋白信号通路抑制OC细胞的增殖、迁移和侵袭，并诱导其凋亡。因此，DEC1可能参与OC的恶性进展，可能成为OC治疗和诊断的靶点。
