Abstract
Gliomas, the most prevalent brain tumors, account for nearly one-third of the all brain and central nervous system (CNS) tumors diagnosed in the USA. The purpose of this study was to discuss the important role of A kinase-interacting protein 1 (AKIP1) in glioma and reveal the potential mechanism. After prediction by CCLE, the expression of AKIP1 was determined by qRT-PCR and western blot. The impacts of AKIP1 knockdown on the proliferation, migration, and invasion were then measured by MTT, colony formation assay, wound healing, and transwell assays. Western blot was used to assess the protein levels of migration and epithelial-mesenchymal transition- (EMT-) related factors. Subsequently, the expression of Disks Large Homolog 2 (DLG2) was predicted by bioinformatics analyses, and the interaction between AKIP1 and DLG2 was confirmed by IP assay, qRT-PCR, and western blot. Finally, DLG2 was further downregulated in glioma cells to detect the association between AKIP1 and DLG2 in the cellular functions of glioma. It was demonstrated that AKIP1 exhibited a high level in glioma cells, and interference of AKIP1 led to reductions in the proliferation, migration, invasion, and EMT of glioma cells. DLG2, which was lowly expressed in glioma cells, demonstrated a negative link to AKIP2. Inhibition of both AKIP2 and DLG2 counteracted the inhibited cellular behaviors on account of AKIP1 interference. To be concluded, this study presented evidence that AKIP1 silencing suppressed the progression of glioma via targeting DLG2, which could provide novel insights to impede the development of glioma.
Highlights
As the most prevalent brain tumor, glioma accounts for nearly one-third of the all brain and central nervous system (CNS) tumors diagnosed in the USA [1, 2]
T98G cells were digested by trypsin and seeded onto 6-well plates overnight to reach 70% confluence. shRNA-A kinase-interacting protein 1 (AKIP1)-1 and shRNAAKIP1-2 vectors were used to silence AKIP1 (GeneCopoeia, Inc.), and sh-Disks Large Homolog 2 (DLG2)-1 and sh-DLG2-2 were used to inhibit DLG2 expression. shRNA-NC served as the corresponding control
AKIP1 Is Highly Expressed in Glioma Cells
Summary
As the most prevalent brain tumor, glioma accounts for nearly one-third of the all brain and central nervous system (CNS) tumors diagnosed in the USA [1, 2]. Due to the difficulties in recognizing their symptoms as a direct outcome of extensive growth and high invasion of glial cells, the patients generally miss the optimal time for treatment [2]. There are some 18,000 people in the USA diagnosed with malignant glioma and 16,000 dies of these diseases every year [3, 4]. The high incidence and mortality, together with the intricate pathogenesis of glioma, call for deepgoing research on the potential drugs or targets for their treatments. A kinase-interacting protein 1 (AKIP1), a 23 kDa protein, was originally discovered in breast and prostate cancer cell lines by mRNA screens [5].
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