title: Potential crosstalk of Ca2+-ROS-dependent mechanism involved in apoptosis of Kasumi-1 cells mediated by heme oxygenase-1 small interfering RNA.
abstract: Acute myeloid leukemia (AML) requires new therapies on the molecular level. Downregulation of heme oxygenase-1 (HO-1) by gene silencing improves the sensitivity of tumor cells to chemotherapy drugs and promotes apoptosis. For the first time, we verified that endoplasmic reticulum and mitochondrial apoptotic pathways were activated by small interfering RNA that targeted-silenced the expression of HO-1 in AML-M2 Kasumi-1 cells. Ca2+ was prone to accumulation and reactive oxygen species were easily generated, while mitochondrial transmembrane potential was reduced. Thus, cytochrome c was released from mitochondria to the cytoplasm and caspases were activated for the following cascade to facilitate apoptosis.
authors.affiliation: Department of Hematology, Affiliated Hospital of Guiyang Medical College, Guiyang 550004, P.R. China.
authors.forename: Sixi
authors.initials: S
authors.lastname: Wei
authors.affiliation: Department of Hematology, Affiliated Hospital of Guiyang Medical College, Guiyang 550004, P.R. China.
authors.forename: Yating
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Hematology, Affiliated Hospital of Guiyang Medical College, Guiyang 550004, P.R. China.
authors.forename: Qixiang
authors.initials: Q
authors.lastname: Chai
authors.affiliation: Department of Pharmacy, Affiliated Hospital of Guiyang Medical College, Guiyang 550004, P.R. China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Fang
authors.affiliation: Department of Hematology, Affiliated Hospital of Guiyang Medical College, Guiyang 550004, P.R. China.
authors.forename: Yaming
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Hematology, Affiliated Hospital of Guiyang Medical College, Guiyang 550004, P.R. China.
authors.forename: Jishi
authors.initials: J
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D002118:Calcium / Q000378:metabolism*; D045744:Cell Line, Tumor; D045304:Cytochromes c / Q000096:biosynthesis; D003630:Daunorubicin / Q000008:administration & dosage; D004721:Endoplasmic Reticulum / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D051547:Heme Oxygenase-1 / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D051379:Mice; D034741:RNA, Small Interfering; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D034741:RNA, Small Interfering; D017382:Reactive Oxygen Species; D045304:Cytochromes c; D051547:Heme Oxygenase-1; D002118:Calcium; D003630:Daunorubicin