
To explore the effect of bortezomib (BOR) on the drug sensitivity of imatinib-resistant chronic myeloid leukemia cell line K562/G01 cell and its mechanism.MTT assay was used to detect the inhibition effect of cell growth, flow cytometry to cell cycle, and real time-PCR to the expression of COX-2 and mdr1 mRNA.Combination of 10 and 20 nmol/L BOR with imatinib could significantly enhance the sensitivity of K562/G01 to imatinib, the reverse factor was 1.83 and 2.72-fold respectively. Cell cycle arrested at G(2)/M phase could be observed by flow cytometry on BOR treatment. The over-expression of COX-2 and mdr1 could be down-regulated by BOR.BOR can enhance the imatinib sensitivity of imatinib resistant K562/G01 cell. The mechanism may be related to cell cycle phase arrested at G2/M and down-regulation of COX-2 and mdr1 expression.
ATP Binding Cassette Transporter, Subfamily B, Cell Cycle, Antineoplastic Agents, Cell Cycle Checkpoints, Boronic Acids, Piperazines, Bortezomib, Pyrimidines, Cyclooxygenase 2, Drug Resistance, Neoplasm, Pyrazines, Benzamides, Imatinib Mesylate, Humans, ATP Binding Cassette Transporter, Subfamily B, Member 1, K562 Cells
ATP Binding Cassette Transporter, Subfamily B, Cell Cycle, Antineoplastic Agents, Cell Cycle Checkpoints, Boronic Acids, Piperazines, Bortezomib, Pyrimidines, Cyclooxygenase 2, Drug Resistance, Neoplasm, Pyrazines, Benzamides, Imatinib Mesylate, Humans, ATP Binding Cassette Transporter, Subfamily B, Member 1, K562 Cells
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