BRG1 promotes progression of B-cell acute lymphoblastic leukemia by disrupting PPP2R1A transcription

Cell Death Dis. 2024 Aug 26;15(8):621. doi: 10.1038/s41419-024-06996-w.

Abstract

Despite advancements in chemotherapy and the availability of novel therapies, the outcome of adult patients with B-cell acute lymphoblastic leukemia (B-ALL) remains unsatisfactory. Therefore, it is necessary to understand the molecular mechanisms underlying the progression of B-ALL. Brahma-related gene 1 (BRG1) is a poor prognostic factor for multiple cancers. Here, the expression of BRG1 was found to be higher in patients with B-ALL, irrespective of the molecular subtype, than in healthy individuals, and its overexpression was associated with a poor prognosis. Upregulation of BRG1 accelerated cell cycle progression into the S phase, resulting in increased cell proliferation, whereas its downregulation facilitated the apoptosis of B-ALL cells. Mechanistically, BRG1 occupies the transcriptional activation site of PPP2R1A, thereby inhibiting its expression and activating the PI3K/AKT signaling pathway to regulate the proto-oncogenes c-Myc and BCL-2. Consistently, silencing of BRG1 and administration of PFI-3 (a specific inhibitor targeting BRG1) significantly inhibited the progression of leukemia and effectively prolonged survival in cell-derived xenograft mouse models of B-ALL. Altogether, this study demonstrates that BRG1-induced overactivation of the PPP2R1A/PI3K/AKT signaling pathway plays an important role in promoting the progression of B-ALL. Therefore, targeting BRG1 represents a promising strategy for the treatment of B-ALL in adults.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • DNA Helicases* / genetics
  • DNA Helicases* / metabolism
  • Disease Progression*
  • Female
  • Humans
  • Male
  • Mice
  • Nuclear Proteins* / genetics
  • Nuclear Proteins* / metabolism
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • Protein Phosphatase 2* / genetics
  • Protein Phosphatase 2* / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / drug effects
  • Transcription Factors* / genetics
  • Transcription Factors* / metabolism
  • Transcription, Genetic / drug effects

Substances

  • DNA Helicases
  • Nuclear Proteins
  • Protein Phosphatase 2
  • Proto-Oncogene Proteins c-akt
  • SMARCA4 protein, human
  • Transcription Factors
  • PPP2R1A protein, human

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