Title:CDK-associated Cullin 1 Promotes Cell Proliferation and Inhibits Cell Apoptosis in Human Glioblastoma
Volume: 21
Issue: 10
关键词:
CACUL1，胶质瘤，增殖，凋亡，CDK2，细胞周期。
摘要:
Background: Glioma is the most common intracranial primary tumour of adult humans,
and its pathological mechanism and molecular characteristics are still under investigation. CDK-associated
cullin 1 (CACUL1) has been shown to regulate colorectal carcinoma, lung cancer, and gastric
cancer development.
Objective: This study aims to explore the role of CACUL1 in the pathogenesis of human glioma.
Methods: CACUL1 levels in human glioma tissue microarrays were detected by immunohistochemistry
analysis. Two glioblastoma cell lines, namely, U87 and U251, were transfected with CACUL1
siRNA, and cell proliferation, cell cycle, cell apoptosis, and regulating molecules, including cyclinE1,
cyclinA2, CDK2, p21, Bcl2, and Bax were assessed by CCK8, flow cytometry, and Western
blot.
Results: CACUL1 expression in glioma tissue was significantly higher than that in normal brain tissue.
CACUL1 knockdown impeded cell proliferation, induced cell apoptosis, and caused G1/S transition
arrest in glioblastoma cells. The cell cycle-related proteins CDK2, cyclinE1, and cyclinA2
were dramatically decreased in the CACUL1 siRNA group compared to the non-targeting siRNA
group in both U87 and U251 cells, while the CDK inhibitory protein p21 was increased in U87
cells. Additionally, the Bcl-2/Bax ratio was significantly decreased.
Conclusion: CACUL1 can promote cell proliferation and suppress apoptosis of glioma cells and
might serve as a potential oncogene for gliomas.
