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. 2022 Jan 24:2022:5648011.
doi: 10.1155/2022/5648011. eCollection 2022.

Silencing of AKIP1 Suppresses the Proliferation, Migration, and Epithelial-Mesenchymal Transition Process of Glioma Cells by Upregulating DLG2

Zhaohui Chen  1 , Haitao Wen  1 , Jinwei Zhang  1 , Xin Zou  1 , Shuihua Wu  1
Affiliations

Silencing of AKIP1 Suppresses the Proliferation, Migration, and Epithelial-Mesenchymal Transition Process of Glioma Cells by Upregulating DLG2

Zhaohui Chen et al. Biomed Res Int. .

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.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
AKIP1 is high expressed in glioma cells. (a) The expression of AKIP1 in glioma was analyzed by CCLE database. (b) and (c) The expression of AKIP1 in normal cell HEB and glioma cell lines was detected by western blot (b) and qRT-PCR (c). ∗∗P < 0.01 and ∗∗∗P < 0.001 vs. HEB.
Figure 2
Figure 2
Silencing AKIP1 suppresses the proliferation of T98G cells. (a) and (b) The protein and mRNA levels of AKIP1 in T98G cells after transfection with corresponding plasmids. (c) The proliferation and (d) colony formation of T98G cells after AKIP1 interference. ∗P < 0.05 and ∗∗∗P < 0.001 vs. shRNA-NC.
Figure 3
Figure 3
Silencing AKIP1 suppresses the migration, invasion, and EMT process of T98G cells. (a) The migration of T98G cells before and after AKIP1 interference was measured by wound healing assay. (b) The invasion of T98G cells before and after AKIP1 interference was detected by transwell assay. (c) The protein levels of migration- and EMT-related factors in T98G cells before and after AKIP1 interference was detected by western blot. ∗∗∗P < 0.001 vs. shRNA-NC.
Figure 4
Figure 4
DLG2 is decreased in glioma cells. (a) The expression of DLG2 in glioma was analyzed by CCLE database. (b) and (c) The expression of DLG2 in normal cell HEB and glioma cell line T98G was detected by western blot (b) and qRT-PCR (c). ∗∗P < 0.01 and ∗∗∗P < 0.001 vs. HEB.
Figure 5
Figure 5
Silencing AKIP1 increases DLG2 expression. (a) and (b) The interaction between AKIP1 and DLG2 expression, as demonstrated by Humanbase and CGGA tools. (c) The binding relationship between AKIP1 and DLG2 was confirmed by IP assay. (d) and (e) The protein level (d) and mRNA level (e) of DLG2 in T98G cells before and after AKIP1 interference. ∗∗∗P < 0.001 vs. shRNA-NC.
Figure 6
Figure 6
Silencing DLG2 reverses the suppressive effects of AKIP1 knockdown on T98G cellular malignant behaviors. (a) and (b) The expression of DLG2 in T98G cells after being knocked down. ∗∗∗P < 0.001 vs. sh-NC. (c) The proliferation, (d) colony formation, (e) and (f) migration, and invasion of T98G cells after AKIP1 and DLG2 interference. (g) The detection of the protein levels of migration- and EMT-related factors in T98G cells after AKIP1 and DLG2 interference by western blot. ∗∗∗P < 0.001 vs. shRNA-NC; ##P < 0.01 and ###P < 0.001 vs. shRNA-AKIP1-2 + sh-NC.
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