Biomaterial Database

Herbimycin A enhances apoptotic effect of chemotherapeutic drugs on K562 cells. 1998

H Ren, and S Chen, and D Lu

Institute of Hematology, People's Hospital, Beijing Medical University, Beijing 100044, China.

OBJECTIVE To explore the anti-apoptotic mechanism and the effective apoptosis-inducing method in chronic myelogenous leukemia (CML) cells. METHODS K562 cell line was used to observe the effect of combination of herbimycin A (HMA), a tyrosine kinase inhibitor, and chemotherapeutic agents on the induction of apoptosis. RESULTS HMA or chemotherapeutic agents could inhibit the proliferation but not significantly induce apoptosis of K562 cells. However, HMA significantly enhanced apoptosis when combined with chemotherapeutic agents. Addition of sulfhydryl compound to the cultures to conjugate HMA completely abrogated this enhancing effect on K562 cells. CONCLUSIONS HMA increases the sensitivity of CML cells to chemotherapeutic agents by inactivating tyrosine kinase activity. It is promising that combination of HMA with conventional chemotherapeutic drugs may be a new strategy in the treatment of CML.

UI	MeSH Term	Description	Entries
D008942	Mitoxantrone	An anthracenedione-derived antineoplastic agent.	Mitozantrone,CL-232325,DHAQ,Mitoxantrone Acetate,Mitoxantrone Hydrochloride,Mitroxone,NSC-279836,NSC-287836,NSC-299195,NSC-301739,NSC-301739D,Novantron,Novantrone,Onkotrone,Pralifan,Ralenova,Acetate, Mitoxantrone,CL 232325,CL232325,Hydrochloride, Mitoxantrone,NSC 279836,NSC 287836,NSC 299195,NSC 301739,NSC 301739D,NSC279836,NSC287836,NSC299195,NSC301739,NSC301739D
D011505	Protein-Tyrosine Kinases	Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.	Tyrosine Protein Kinase,Tyrosine-Specific Protein Kinase,Protein-Tyrosine Kinase,Tyrosine Kinase,Tyrosine Protein Kinases,Tyrosine-Specific Protein Kinases,Tyrosylprotein Kinase,Kinase, Protein-Tyrosine,Kinase, Tyrosine,Kinase, Tyrosine Protein,Kinase, Tyrosine-Specific Protein,Kinase, Tyrosylprotein,Kinases, Protein-Tyrosine,Kinases, Tyrosine Protein,Kinases, Tyrosine-Specific Protein,Protein Kinase, Tyrosine-Specific,Protein Kinases, Tyrosine,Protein Kinases, Tyrosine-Specific,Protein Tyrosine Kinase,Protein Tyrosine Kinases,Tyrosine Specific Protein Kinase,Tyrosine Specific Protein Kinases
D011809	Quinones	Hydrocarbon rings which contain two ketone moieties in any position. They can be substituted in any position except at the ketone groups.
D005047	Etoposide	A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.	Demethyl Epipodophyllotoxin Ethylidine Glucoside,Celltop,Eposide,Eposin,Eto-GRY,Etomedac,Etopos,Etoposide Pierre Fabre,Etoposide Teva,Etoposide, (5S)-Isomer,Etoposide, (5a alpha)-Isomer,Etoposide, (5a alpha,9 alpha)-Isomer,Etoposide, alpha-D-Glucopyranosyl Isomer,Etoposido Ferrer Farma,Exitop,Lastet,NSC-141540,Onkoposid,Riboposid,Toposar,VP 16-213,VP-16,Vepesid,Vépéside-Sandoz,Eto GRY,Etoposide, alpha D Glucopyranosyl Isomer,NSC 141540,NSC141540,Teva, Etoposide,VP 16,VP 16 213,VP 16213,VP16,Vépéside Sandoz,alpha-D-Glucopyranosyl Isomer Etoposide
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000903	Antibiotics, Antineoplastic	Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.	Antineoplastic Antibiotics,Cytotoxic Antibiotics,Antibiotics, Cytotoxic
D000971	Antineoplastic Combined Chemotherapy Protocols	The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.	Anticancer Drug Combinations,Antineoplastic Agents, Combined,Antineoplastic Chemotherapy Protocols,Antineoplastic Drug Combinations,Cancer Chemotherapy Protocols,Chemotherapy Protocols, Antineoplastic,Drug Combinations, Antineoplastic,Antineoplastic Combined Chemotherapy Regimens,Combined Antineoplastic Agents,Agent, Combined Antineoplastic,Agents, Combined Antineoplastic,Anticancer Drug Combination,Antineoplastic Agent, Combined,Antineoplastic Chemotherapy Protocol,Antineoplastic Drug Combination,Cancer Chemotherapy Protocol,Chemotherapy Protocol, Antineoplastic,Chemotherapy Protocol, Cancer,Chemotherapy Protocols, Cancer,Combinations, Antineoplastic Drug,Combined Antineoplastic Agent,Drug Combination, Anticancer,Drug Combination, Antineoplastic,Drug Combinations, Anticancer,Protocol, Antineoplastic Chemotherapy,Protocol, Cancer Chemotherapy,Protocols, Antineoplastic Chemotherapy,Protocols, Cancer Chemotherapy
D013713	Teniposide	A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle.	Demethyl Epipodophyllotoxin Thenylidine Glucoside,NSC-122819,Teniposide, (5a alpha,9 alpha(S*))-Isomer,VM-26,Vumon,NSC 122819,NSC122819,VM 26,VM26
D016227	Benzoquinones	Benzene rings which contain two ketone moieties in any position. They can be substituted in any position except at the ketone groups.	1,2-Benzoquinones,1,4-Benzoquinones,Benzodiones,2,5-Cyclohexadiene-1,4-Diones,o-Benzoquinones,p-Benzoquinones
D017209	Apoptosis	A regulated cell death mechanism characterized by distinctive morphologic changes in the nucleus and cytoplasm, including the endonucleolytic cleavage of genomic DNA, at regularly spaced, internucleosomal sites, i.e., DNA FRAGMENTATION. It is genetically programmed and serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.	Apoptosis, Extrinsic Pathway,Apoptosis, Intrinsic Pathway,Caspase-Dependent Apoptosis,Classic Apoptosis,Classical Apoptosis,Programmed Cell Death,Programmed Cell Death, Type I,Apoptoses, Extrinsic Pathway,Apoptoses, Intrinsic Pathway,Apoptosis, Caspase-Dependent,Apoptosis, Classic,Apoptosis, Classical,Caspase Dependent Apoptosis,Cell Death, Programmed,Classic Apoptoses,Extrinsic Pathway Apoptoses,Extrinsic Pathway Apoptosis,Intrinsic Pathway Apoptoses,Intrinsic Pathway Apoptosis