期刊
BIOLOGICAL & PHARMACEUTICAL BULLETIN
卷 46, 期 9, 页码 1304-1309出版社
PHARMACEUTICAL SOC JAPAN
关键词
K562/ADM; buthionine sulfoximine; glutathione; drug resistance
This study found that the expression of solute carrier (SLC) family member SLC25A40 was up-regulated in doxorubicin-resistant K562/ADM cells, which affected cell proliferation and drug resistance to ADM.
The chronic myelogenous leukemia cell line, K562/ADM is derived from the K562 cell line, which is re-sistant to doxorubicin (alias, adriamycin: ADM). P-glycoprotein levels are significantly higher in K562/ADM cells than in K562 cells. The overexpression of p-glycoprotein has been shown to cause drug resistance. Therefore, the present study investigated a novel mechanism underlying the drug resistance of K562/ADM cells. A gene ontology analysis demonstrated that the expression of solute carrier (SLC)-mediated transmem-brane transport genes was significantly higher in K562/ADM cells than in K562 cells. The expression level of a member of the SLC family, SLC25A40 was higher in K562/ADM cells than in K562 cells. SLC25A40 is lo-cated near the ABCB1 gene. A real-time PCR analysis showed that the expression of SLC25A40, ABCB4, and ADAM22 was up-regulated. These genes are located close to SLC25A40. The down-regulation of SLC25A40 significantly decreased the mitochondrial concentration of glutathione and cell proliferation. Collectively, the present results demonstrated that the expression of SLC25A40 was up-regulated in K562/ADM cells, which enhanced to cell proliferation, and that the expression of SLC25A40 affected drug resistance to ADM.
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