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

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. Af...

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Publicado en:BioMed Research International pp. 1 - 13
Autores principales: Chen, Zhaohui, Wen, Haitao, Zhang, Jinwei, Zou, Xin, Wu, Shuihua
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell 1/24/2022
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 1/24/2022
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1155/2022/5648011
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        atl: Silencing of AKIP1 Suppresses the Proliferation, Migration, and Epithelial-Mesenchymal Transition Process of Glioma Cells by Upregulating DLG2.
      aug:
        au:
          Chen, Zhaohui
          Wen, Haitao
          Zhang, Jinwei
          Zou, Xin
          Wu, Shuihua
        affil: Department of Neurosurgery, Hunan Children's Hospital, Changsha City, 410000 Hunan Province, China
      sug:
        subj:
          Cell Proliferation
          Epithelial-Mesenchymal Transition
          Glioma
          Cell Line, Tumor
          Carrier Proteins Metabolism
          Human
          Reverse Transcriptase Polymerase Chain Reaction
          Blotting, Western
          Neoplasm Invasiveness
          Wound Healing
          Bioinformatics
          Disease Progression
      ab: 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.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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