Knockdown of ADAMDEC1 inhibits the progression of glioma in vitro.

Abstract

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.