Liu Xueliang, Huang Hao, Li Xuehan, Zheng Xiaomei, Zhou Chong, Xue Bin, He Jimin, Zhang Ye, Liu Liang
Department of Neurosurgery, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Department of Neurosurgery, Guang'an People's Hospital, Guangan, Sichuan, China.
Histol Histopathol. 2020 Sep;35(9):997-1005. doi: 10.14670/HH-18-227. Epub 2020 May 6.
Glioma is one of the most lethal malignant tumors all over the world. The prognosis of patients with high‑grade glioma remains very poor. Therefore, it is urgent to find a novel strategy for the treatment of glioma. It has been reported that ADAMDEC1 could regulate the progression of multiple diseases, including cancers. However, the role of ADAMDEC1 during the tumorigenesis of glioma remains largely unknown. Methods, Gene expression of ADAMDEC1 in glioma tissues or in cells was detected by qRT-PCR. Western blot was performed to measure the protein expressions of p53, active caspase3, active caspase9, CDK2 and Cyclin A in glioma cells. Cell proliferation was detected by CCK-8 assay. Cell apoptosis or cycle was tested by flow cytometry. Transwell was used to test the invasion of glioma cells.
The expression of ADAMDEC1 in glioma tissues or cells was significantly upregulated. In addition, downregulation of ADAMDEC1 notably inhibited the proliferation and induced apoptosis of glioma cells through upregulation of active caspase 3 and active caspase 9. Besides, silencing of ADAMDEC1 obviously induced G1 arrest in glioma cells via modulation of cell cycle-related proteins. Finally, knockdown of ADAMDEC1 significantly inhibited the migration and invasion of glioma cells. In contrast, overexpression of ADAMDEC1 promoted cell proliferation, migration and invasion of glioma cells.
Downregulation of ADAMDEC1 could significantly inhibit the tumorigenesis of glioma in vitro, which may serve as a novel target for the treatment of glioma.
胶质瘤是全球最致命的恶性肿瘤之一。高级别胶质瘤患者的预后仍然很差。因此，迫切需要找到一种新的胶质瘤治疗策略。据报道，ADAMDEC1可调节包括癌症在内的多种疾病的进展。然而，ADAMDEC1在胶质瘤发生过程中的作用仍 largely未知。方法：通过qRT-PCR检测胶质瘤组织或细胞中ADAMDEC1的基因表达。进行蛋白质印迹法以测量胶质瘤细胞中p53、活性caspase3、活性caspase9、CDK2和细胞周期蛋白A的蛋白质表达。通过CCK-8测定法检测细胞增殖。通过流式细胞术检测细胞凋亡或周期。使用Transwell检测胶质瘤细胞的侵袭。
ADAMDEC1在胶质瘤组织或细胞中的表达显著上调。此外，ADAMDEC1的下调通过上调活性caspase 3和活性caspase 9显著抑制胶质瘤细胞的增殖并诱导其凋亡。此外，ADAMDEC1的沉默通过调节细胞周期相关蛋白明显诱导胶质瘤细胞中的G1期阻滞。最后，ADAMDEC1的敲低显著抑制胶质瘤细胞的迁移和侵袭。相反，ADAMDEC1的过表达促进胶质瘤细胞的增殖、迁移和侵袭。
ADAMDEC1的下调可在体外显著抑制胶质瘤的发生，这可能成为胶质瘤治疗的新靶点。
