TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000345358
  • Gene Name:BAX
  • mRNA database:Ensembl
  • mRNA expression :up-regulated
  • mRNA Method:qRT-PCR
  • mRNA Pathway:apoptotic signaling pathway
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:NA
  • Drug Name:Realgar
  • Drug Method:up-regulated the gene expression

Disease basic infommation

  • Disease:chronic lymphocytic leukemia
  • Tissue:cell line (MEC-1)

Other information

  • Title:Realgar induces apoptosis in the chronic lymphocytic leukemia cell line MEC1
  • Journal:Mol Med Rep
  • Published:2013
  • PubMed ID:24141727
  • Abstract:The aim of the present study was to investigate the effect of realgar on the viability, proliferation and apoptosis in the human chronic lymphocytic leukemia (CLL) cell line, MEC-1. Potential mechanisms mediating the effect were also explored in the experiment. Cultured MEC-1 cells were incubated with various concentrations of realgar for 24, 48 and 72 h. A WST-8 assay was employed to evaluate the effect on cell viability. Inhibitory effects on cell proliferation were determined using a 5-bromodeoxyuridine cell proliferation ELISA. The apoptotic effect on MEC-1 cells was evaluated by annexin V-fluorescein isothiocyanate/propidium iodide dual staining, followed by flow cytometry. Quantitative polymerase chain reaction was performed to determine the mRNA expression levels of BCL2-associated X protein (BAX), BCL2-like 1 (Bcl-xL), v-myc myelocytomatosis viral oncogene homolog (avian; c-Myc) and cyclin-dependent kinase inhibitor 1A (p21). It was found that viability and proliferation were significantly reduced while apoptotic rates increased in MEC-1 cells following exposure to realgar. Furthermore, mRNA expression of BAX and c-Myc was upregulated and downregulated, respectively, in realgar-treated MEC-1 cells. In conclusion, the results showed that realgar inhibits viability and prolife-ration and induces apoptosis of MEC-1 cells in a dose- and time-dependent manner. The effect may depend on the mitochondrial apoptosis pathway. The results of the present study may be beneficial in the identification of a new target therapy for CLL.
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