Geldanamycin induces cell cycle arrest in K562 erythroleukemic cells.

H R Kim, C H Lee, Y H Choi, H S Kang, H D Kim
Author Information
  1. H R Kim: Department of Molecular Biology, College of Natural Sciences, Pusan National University, Korea.

Abstract

Geldanamycin (GA), a benzoquinone ansamycin, is one of the specific inhibitors of 90-kDa heat shock protein and induces growth inhibition and apoptosis in certain cancer cell lines. We have investigated the mechanism of GA-induced growth inhibition in K562 erythroleukemic cells. DNA flow-cytometric analysis indicated that GA-induced growth arrest was associated with G2/M phase arrest of the cell cycle. GA treatment down-regulated the expression of cyclin B1 and inhibited phosphorylation of Cdc2 protein, both key regulatory proteins at the G2/M boundary. GA also markedly inhibited the Cdc2 kinase activity, which may be in part a result of up-regulation of p27KIP1 by GA. The present results suggest a novel mechanism that p27KIP1 could be involved in the regulation of G2 to M phase transition.

MeSH Term

Antibiotics, Antineoplastic
Benzoquinones
CDC2 Protein Kinase
Cell Cycle
Cell Cycle Proteins
Cell Division
Cyclin B
Cyclin B1
Cyclin-Dependent Kinase Inhibitor p27
G2 Phase
Growth Inhibitors
Humans
K562 Cells
Lactams, Macrocyclic
Leukemia, Erythroblastic, Acute
Microtubule-Associated Proteins
Mitosis
Phosphorylation
Quinones
Tumor Suppressor Proteins
Up-Regulation

Chemicals

Antibiotics, Antineoplastic
Benzoquinones
CCNB1 protein, human
Cell Cycle Proteins
Cyclin B
Cyclin B1
Growth Inhibitors
Lactams, Macrocyclic
Microtubule-Associated Proteins
Quinones
Tumor Suppressor Proteins
Cyclin-Dependent Kinase Inhibitor p27
CDC2 Protein Kinase
geldanamycin

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