Knockdown of BCL6 Inhibited Malignant Phenotype and Enhanced Sensitivity of Glioblastoma Cells to TMZ through AKT Pathway.

Background. BCL6 was a critical prooncogene of human B-cell lymphomas which promoted tumor progress and contributed to malignant behavior in several kinds of cancers. This study was to detect the expression of BCL6 and its biological effect on glioma. Methods. RT-PCR and Western blot were used to de...

Descripción completa

Detalles Bibliográficos
Publicado en:BioMed Research International pp. 1 - 12
Autores principales: Song, Wen, Wang, Zhenling, Kan, Pengcheng, Ma, Zhuolin, Wang, Yaru, Wu, Qiaoli, Yao, Xiuhua, Zhang, Biao
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell 10/18/2018
Acceso en línea:Ver este registro en EBSCOhost
fields @attributes:
  recordID: 1
pdfLink:
plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=132506387&site=ehost-live
header:
  @attributes:
    shortDbName: ccm
    uiTerm: 132506387
    longDbName: CINAHL Complete
    uiTag: AN
  controlInfo:
    bkinfo:
    dissinfo:
    jinfo:
      jid:
        23146133
        FT2T
      jtl: BioMed Research International
      issn: 23146133
      maglogo: N
    pubinfo:
      dt: 10/18/2018
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
    artinfo:
      ui:
        132506387
        132506387
        132506387
        10.1155/2018/6953506
        132506387
      ppf: 1
      ppct: 11
      formats:
        fmt:
          – @attributes:
              type: T
          – @attributes:
              type: P
      tig:
        atl: Knockdown of BCL6 Inhibited Malignant Phenotype and Enhanced Sensitivity of Glioblastoma Cells to TMZ through AKT Pathway.
      aug:
        au:
          Song, Wen
          Wang, Zhenling
          Kan, Pengcheng
          Ma, Zhuolin
          Wang, Yaru
          Wu, Qiaoli
          Yao, Xiuhua
          Zhang, Biao
        affil: The Graduate School, Tianjin Medical University, Tianjin 300070, China
      sug:
        subj:
          Transcription Factors Pharmacodynamics
          Phenotype Drug Effects
          Glioma Familial and Genetic
          Cell Line, Tumor Drug Effects
          Temozolomide Drug Effects
          Protein Kinases Drug Effects
          Signal Transduction Drug Effects
          Gene Expression
          Genetic Techniques Methods
          Oncogenes
          Human
          Reverse Transcriptase Polymerase Chain Reaction
          Blotting, Western
          RNA, Messenger
          RNA
          Cell Count
          Colony-Forming Units Assay
          Flow Cytometry
          Wound Healing
          Neoplasm Staging
          Cell Proliferation Drug Effects
          Cell Movement Drug Effects
          Neoplasm Invasiveness
          Biochemical Phenomena Drug Effects
          Cell Cycle Proteins Drug Effects
          Matrix Metalloproteinases Drug Effects
      ab: Background. BCL6 was a critical prooncogene of human B-cell lymphomas which promoted tumor progress and contributed to malignant behavior in several kinds of cancers. This study was to detect the expression of BCL6 and its biological effect on glioma. Methods. RT-PCR and Western blot were used to detect the expression of BCL6 mRNA and protein in tissues and glioblastoma cell lines. The expression of BCL6 was knockdown in two glioblastoma cell lines (U87 and U251) using BCL6 shRNA. The CCK8, colony-formation, flow cytometry, Transwell, and wound-healing assays were used to evaluate the malignant phenotypic change of glioblastoma cells. Results. The expression of BCL6 was higher in glioma tissues and glioblastoma cell lines than normal tissues. Knockdown of BCL6 expression reduced the proliferation, migration, and invasion of glioblastoma cells. Moreover, knockdown of BCL6 changed expression of proteins related to malignant behaviors of glioblastoma cells. The suppression of BCL6 could increase chemosensitivity of U87 and U251 to temozolomide. Downregulation of BCL6 levels suppressed the expression of BCL2, cyclin D1, MMP2, and MMP9 proteins as well as two classic signaling pathway proteins p-AKT and p-ERK. Simultaneously, BAX and p21 protein levels were upregulated along with knockdown of BCL6. Conclusions. Our results indicated that BCL6 may be a tumor oncogene involved in the progression of glioma via affecting AKT and MAPK signaling pathways.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
    refInfo:
    holdings:
      @attributes:
        islocal: N