Abstract
BackgroundGlioblastoma (GBM) is the most common primary malignant brain tumor in adults with a poor prognosis. DEPDC1B (DEP domain-containing protein 1B) has been shown to be associated with some types of malignancies. However, the role and underlying regulatory mechanisms of DEPDC1B in GBM remain elusive.MethodsIn this research, the expression level of DEPDC1B in GBM tissues was detected by IHC. The DEPDC1B knockdown cell line was constructed, identified by qRT-PCR and western blot and used to construct the xenotransplantation mice model and intracranial xenograft model. MTT assay, colony formation assay, flow cytometry, and Transwell assay were used to detected cell proliferation, apoptosis and migration.ResultsThe results proved that DEPDC1B was significantly upregulated in tumor tissues, and silencing DEPDC1B could inhibit proliferation, migration and promote apoptosis of GBM cell. In addition, human apoptosis antibody array detection showed that after DEPDC1B knockdown, the expression of apoptosis-related proteins was downregulated, such as IGFBP-2, Survivin, N-cadherin, Vimentin and Snail. Finally, we indicated that knockdown of DEPDC1B significantly inhibited tumor growth in vivo.ConclusionsIn summary, DEPDC1B was involved in the development and progression of GBM, which may be a potential therapeutic target and bring a breakthrough in the treatment.
Highlights
Glioblastoma multiforme (GBM) is a lethal malignancy of the central nervous system (CNS) [1], accounting for approximately 15% of all primary brain tumors and 60% of all astrocytomas [2]
DEP domain-containing protein 1B (DEPDC1B) is upregulated in GBM patients First, results of Immunohistochemical staining (IHC) shown that the expression of DEPDC1B in the tumor tissues was significantly higher than that in the normal tissues (Fig. 1a)
Based on Mann–Whitney U analysis (Table 1), we found that the significant correlation between DEPDC1B expression and pathological grading as well as tumor recurrence
Summary
Glioblastoma multiforme (GBM) is a lethal malignancy of the central nervous system (CNS) [1], accounting for approximately 15% of all primary brain tumors and 60% of all astrocytomas [2]. The treatment of GBM is mainly tumor resection, followed by adjuvant radiotherapy and temozolomide [3]. This standardized treatment has shown effectiveness in extending patient survival, the prognosis is still extremely poor, with a median survival (MS) of 14.6 months and an average 5-year survival of less than 5% [1, 4, 5]. Glioblastoma (GBM) is the most common primary malignant brain tumor in adults with a poor progno‐ sis. The role and underlying regulatory mechanisms of DEPDC1B in GBM remain elusive
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