Deregulation of Mitochondrial ATPsyn- beta in Acute Myeloid Leukemia Cells and with Increased Drug Resistance: e83610
The mechanisms underlying the development of multidrug resistance in acute myeloid leukemia are not fully understood. Here we analyzed the expressions of mitochondrial ATPsyn- beta in adriamycin-resistant cell line HL-60/ADM and its parental cell line HL-60. Meanwhile we compared the differences of...
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| Veröffentlicht in: | PloS one 2013-12, Vol.8 (12) |
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| creator | Xiao, Xiang Yang, Jingke Li, Ruijuan Liu, Sufang Xu, Yunxiao Zheng, Wenli Yi, Yan Luo, Yunya Gong, Fanjie Peng, Honglin |
| description | The mechanisms underlying the development of multidrug resistance in acute myeloid leukemia are not fully understood. Here we analyzed the expressions of mitochondrial ATPsyn- beta in adriamycin-resistant cell line HL-60/ADM and its parental cell line HL-60. Meanwhile we compared the differences of mitochondrial ATPsyn- beta expression and ATP synthase activity in 110 acute myeloid leukemia (AML, non-M3) patients between relapsed/refractory and those in remission. Our results showed that down-regulation of ATPsyn- beta expression by siRNA in HL-60 cells increased cell viability and apoptotic resistance to adriamycin, while up-regulation of mitochondrial ATPsyn- beta in HL-60/ADM cells enhanced cell sensitivity to adriamycin and promoted apoptosis. Mitochondrial ATPsyn- beta expression and ATP synthase activity in relapsed/refractory acute myeloid leukemia patients were downregulated. This downregulated ATPsyn- beta expression exhibited a positive correlation with the response to adriamycin of primary cells. A lower expression of ATPsyn- beta in newly diagnosed or relapsed/refractory patients was associated with a shorter first remission duration or overall survival. Our findings show mitochondrial ATPsyn- beta plays an important role in the mechanism of multidrug resistance in AML thus may present both a new marker for prognosis assessment and a new target for reversing drug resistance. |
| doi_str_mv | 10.1371/journal.pone.0083610 |
| format | Article |
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Here we analyzed the expressions of mitochondrial ATPsyn- beta in adriamycin-resistant cell line HL-60/ADM and its parental cell line HL-60. Meanwhile we compared the differences of mitochondrial ATPsyn- beta expression and ATP synthase activity in 110 acute myeloid leukemia (AML, non-M3) patients between relapsed/refractory and those in remission. Our results showed that down-regulation of ATPsyn- beta expression by siRNA in HL-60 cells increased cell viability and apoptotic resistance to adriamycin, while up-regulation of mitochondrial ATPsyn- beta in HL-60/ADM cells enhanced cell sensitivity to adriamycin and promoted apoptosis. Mitochondrial ATPsyn- beta expression and ATP synthase activity in relapsed/refractory acute myeloid leukemia patients were downregulated. This downregulated ATPsyn- beta expression exhibited a positive correlation with the response to adriamycin of primary cells. A lower expression of ATPsyn- beta in newly diagnosed or relapsed/refractory patients was associated with a shorter first remission duration or overall survival. Our findings show mitochondrial ATPsyn- beta plays an important role in the mechanism of multidrug resistance in AML thus may present both a new marker for prognosis assessment and a new target for reversing drug resistance.</description><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0083610</identifier><language>eng</language><ispartof>PloS one, 2013-12, Vol.8 (12)</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,27924,27925</link.rule.ids></links><search><creatorcontrib>Xiao, Xiang</creatorcontrib><creatorcontrib>Yang, Jingke</creatorcontrib><creatorcontrib>Li, Ruijuan</creatorcontrib><creatorcontrib>Liu, Sufang</creatorcontrib><creatorcontrib>Xu, Yunxiao</creatorcontrib><creatorcontrib>Zheng, Wenli</creatorcontrib><creatorcontrib>Yi, Yan</creatorcontrib><creatorcontrib>Luo, Yunya</creatorcontrib><creatorcontrib>Gong, Fanjie</creatorcontrib><creatorcontrib>Peng, Honglin</creatorcontrib><title>Deregulation of Mitochondrial ATPsyn- beta in Acute Myeloid Leukemia Cells and with Increased Drug Resistance: e83610</title><title>PloS one</title><description>The mechanisms underlying the development of multidrug resistance in acute myeloid leukemia are not fully understood. Here we analyzed the expressions of mitochondrial ATPsyn- beta in adriamycin-resistant cell line HL-60/ADM and its parental cell line HL-60. Meanwhile we compared the differences of mitochondrial ATPsyn- beta expression and ATP synthase activity in 110 acute myeloid leukemia (AML, non-M3) patients between relapsed/refractory and those in remission. Our results showed that down-regulation of ATPsyn- beta expression by siRNA in HL-60 cells increased cell viability and apoptotic resistance to adriamycin, while up-regulation of mitochondrial ATPsyn- beta in HL-60/ADM cells enhanced cell sensitivity to adriamycin and promoted apoptosis. Mitochondrial ATPsyn- beta expression and ATP synthase activity in relapsed/refractory acute myeloid leukemia patients were downregulated. This downregulated ATPsyn- beta expression exhibited a positive correlation with the response to adriamycin of primary cells. A lower expression of ATPsyn- beta in newly diagnosed or relapsed/refractory patients was associated with a shorter first remission duration or overall survival. 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Here we analyzed the expressions of mitochondrial ATPsyn- beta in adriamycin-resistant cell line HL-60/ADM and its parental cell line HL-60. Meanwhile we compared the differences of mitochondrial ATPsyn- beta expression and ATP synthase activity in 110 acute myeloid leukemia (AML, non-M3) patients between relapsed/refractory and those in remission. Our results showed that down-regulation of ATPsyn- beta expression by siRNA in HL-60 cells increased cell viability and apoptotic resistance to adriamycin, while up-regulation of mitochondrial ATPsyn- beta in HL-60/ADM cells enhanced cell sensitivity to adriamycin and promoted apoptosis. Mitochondrial ATPsyn- beta expression and ATP synthase activity in relapsed/refractory acute myeloid leukemia patients were downregulated. This downregulated ATPsyn- beta expression exhibited a positive correlation with the response to adriamycin of primary cells. A lower expression of ATPsyn- beta in newly diagnosed or relapsed/refractory patients was associated with a shorter first remission duration or overall survival. Our findings show mitochondrial ATPsyn- beta plays an important role in the mechanism of multidrug resistance in AML thus may present both a new marker for prognosis assessment and a new target for reversing drug resistance.</abstract><doi>10.1371/journal.pone.0083610</doi></addata></record> |
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| title | Deregulation of Mitochondrial ATPsyn- beta in Acute Myeloid Leukemia Cells and with Increased Drug Resistance: e83610 |
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