title: Realgar induces apoptosis in the chronic lymphocytic leukemia cell line MEC‑1.
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.
authors.affiliation: Department of Hematology, Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.
authors.forename: Xinyu
authors.initials: X
authors.lastname: Liu
authors.forename: Xianglu
authors.initials: X
authors.lastname: Li
authors.forename: Ling
authors.initials: L
authors.lastname: Wang
authors.forename: Xiao
authors.initials: X
authors.lastname: Lv
authors.forename: Na
authors.initials: N
authors.lastname: Chen
authors.forename: Peipei
authors.initials: P
authors.lastname: Li
authors.forename: Kang
authors.initials: K
authors.lastname: Lu
authors.forename: Xin
authors.initials: X
authors.lastname: Wang
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D001152:Arsenicals / Q000494:pharmacology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects / Q000235:genetics; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects / Q000235:genetics; D004354:Drug Screening Assays, Antitumor; D015973:Gene Expression Regulation, Leukemic / Q000187:drug effects; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000235:genetics / Q000473:pathology*; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013440:Sulfides / Q000494:pharmacology*; D014158:Transcription, Genetic / Q000187:drug effects; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism; D051020:bcl-X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: D001152:Arsenicals; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016271:Proto-Oncogene Proteins c-myc; D012333:RNA, Messenger; D013440:Sulfides; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; C058317:arsenic disulfide