title: Realgar-induced apoptosis and differentiation in all-trans retinoic             acid (ATRA)-sensitive NB4 and ATRA-resistant MR2 cells.
abstract: Realgar has been used in Western medicine and Chinese traditional medicine             since ancient times, and its promising anticancer activity has attracted much             attention in recent years, especially for acute promyelocytic leukemia (APL).             However, the therapeutic action of realgar treatment for APL remains to be fully             elucidated. Cellular cytotoxicity, proliferation, apoptosis and differentiation             were comprehensively investigated in realgar-treated cell lines derived from PML-RARα+             APL patient, including the all-trans retinoic acid (ATRA)-sensitive NB4 and ATRA-resistant             MR2 cell lines. For analysis of key regulators of apoptosis and differentiation,             gene expression profiles were performed in NB4 cells. Realgar was found to induce             apoptosis and differentiation in both cell lines, and these effects were exerted             simultaneously. Gene expression profiles indicated that genes influenced by realgar             treatment were involved in the modulation of signal transduction, translation,             transcription, metabolism and the immune response. Given its low toxicity, realgar             is a promising alternative reagent for the therapy of APL. Our data contribute             to an understanding of the underlying mechanism responsible for the therapeutic             effects of realgar in the clinical treatment of APL.
authors: Department of Oncology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, PR China. siyu.chen@shsmu.edu.cn
authors: Siyu
authors: S
authors: Chen
authors: Yi
authors: Y
authors: Fang
authors: Liheng
authors: L
authors: Ma
authors: Shanxi
authors: S
authors: Liu
authors: Xinmin
authors: X
authors: Li
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D001152:Arsenicals / Q000494:pharmacology*; D002454:Cell Differentiation / Q000187:drug effects; D045744:Cell Line, Tumor; D004273:DNA, Neoplasm / Q000032:analysis / Q000235:genetics; D018572:Disease-Free Survival; D020869:Gene Expression Profiling; D006801:Humans; D015473:Leukemia, Promyelocytic, Acute / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D046228:Microarray Analysis; D015514:Oncogene Proteins, Fusion / Q000378:metabolism; D015398:Signal Transduction; D013440:Sulfides / Q000494:pharmacology*; D014212:Tretinoin / Q000494:pharmacology*
chemical_list: D001152:Arsenicals; D004273:DNA, Neoplasm; D015514:Oncogene Proteins, Fusion; D013440:Sulfides; C093476:promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; C058317:arsenic disulfide; D014212:Tretinoin