BRG1 regulation by miR-155 in human leukemia and lymphoma cell lines

Clin Transl Oncol. 2017 Aug;19(8):1010-1017. doi: 10.1007/s12094-017-1633-2. Epub 2017 Mar 1.

Abstract

Introduction/purpose: BRG1 is a key regulator of leukemia stem cells. Indeed, it has been observed that this type of cells is unable to divide, survive and develop new tumors when BRG1 is down-regulated.

Materials and methods: We assessed BRG1 and miR-155 expression in 23 leukemia cell lines, and two no pathological lymphocyte samples using qPCR. MiR-155 transfection and western blot were used to analyze the relationship between miR-155 and its validated target, BRG1, by measuring protein expression levels. The effect of miR-155 on cell proliferation and prednisolone sensitivity were studied with resazurin assay.

Results: BRG1 expression levels could correlate negatively with miR-155 expression levels, at least in Burkitt's lymphoma and diffuse large B cell lymphoma (DLBCL) cell lines. To clarify the role of miR-155 in the regulation of BRG1 expression, we administrated miR-155 mimics in different leukemia/lymphoma cell lines. Our results suggest that miR-155 regulate negatively and significantly the BRG1 expression at least in the MOLT4 cell line.

Conclusion: Our study revealed a previously unknown miR-155 heterogeneity that could result in differences in the treatment with miRNAs in our attempt to inhibit BRG1. However, the expression levels of BRG1 and miR-155, before prednisolone treatment were not statistically significantly associated prednisolone sensitive leukemia cells.

Keywords: BRG1; Leukemia; Prednisolone; miR-155.

MeSH terms

  • Cell Proliferation*
  • DNA Helicases / genetics
  • DNA Helicases / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Leukemia / genetics
  • Leukemia / metabolism
  • Leukemia / pathology*
  • Lymphoma / genetics
  • Lymphoma / metabolism
  • Lymphoma / pathology*
  • MicroRNAs / genetics*
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Tumor Cells, Cultured

Substances

  • MIRN155 microRNA, human
  • MicroRNAs
  • Nuclear Proteins
  • Transcription Factors
  • SMARCA4 protein, human
  • DNA Helicases