Xueliang Liu1,2, Hao Huang1, Xuehan Li3, Xiaomei Zheng4, Chong Zhou5, Bin Xue6, Jimin He7, Ye Zhang8, Liang Liu1,9,10. 1. Department of Neurosurgery, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China. 2. Department of Neurology, First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, China. 3. Department of Neurosurgery, Guang 'an People's Hospital, Guangan, Sichuan, China. 4. Department of Neurology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China. 5. Department of Neurology, Jianyang People's Hospital, Jianyang, Sichuan, China. 6. Department of Neurosurgery, Nanbu People's Hospital, Nanchong, Sichuan, China. 7. Department of Neurosurgery, Suining Central Hospital, Suining, Sichuan, China. 8. Department of Neurosurgery, Mianyang Central Hospital, Mianyang, Sichuan, China. 9. Neurosurgery Clinical Medical Research Center of Sichuan Province, Chengdu, Sichuan, China. 10. Academician (expert) Workstation of Sichuan Province, Chengdu, Sichuan, China. liuliangl_1234@126.com.
Abstract
BACKGROUND: 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. RESULTS: 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. CONCLUSION: Downregulation of ADAMDEC1 could significantly inhibit the tumorigenesis of glioma in vitro, which may serve as a novel target for the treatment of glioma.
BACKGROUND: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. RESULTS: 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. CONCLUSION: Downregulation of ADAMDEC1 could significantly inhibit the tumorigenesis of glioma in vitro, which may serve as a novel target for the treatment of glioma.
Authors: Weiliang Zhu; Lin Shi; Yuxin Gong; Lin Zhuo; Siyun Wang; Shaobing Chen; Bei Zhang; Bin Ke Journal: Thorac Cancer Date: 2022-02-17 Impact factor: 3.500