Combination of galectin inhibitor GCS-100 and BH3 mimetics eliminates both p53 wild type and p53 null AML cells
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- 作者：Peter P. Ruvoloa ; pruvolo@mdanderson.org" class="auth_mail" title="E-mail the corresponding author ; Vivian R. Ruvoloa ; Christopher B. Bentona ; Ahmed AlRawia ; Jared K. Burksa ; Wendy Schobera ; James Rolkec ; George Tidmarshc ; Numsen Hail Jra ; R. Eric Davisb ; Michael Andreeffa
- 关键词：LGALS3 ; Galectin 3 ; LGALS1 ; Galectin 1 ; AML ; Acute myeloid leukemia ; qRT-PCR ; Real-time PCR ; AKT ; Protein kinase B ; ERK ; Extracellular receptor kinase ; BCL2 ; B cell lymphoma 2 ; BCL-XL ; B cell lymphoma 2 Like 1 ; MCL-1 ; Myeloid cell leukemia 1 ; Ph ; + ; ; Philadelphia chromosome + ; ; ALL ; Acute lymphoblastic leukemia ; GSK3 ; Glycogen synthase kinase 3 ; TET1 ; Ten&ndash ; eleven translocation 1 ; NPM1 ; Nucleophosmin 1 ; FANCD2 ; Fanconi Anemia Complementation Group D2 ; GCN2 ; General control nond
- 刊名：Biochimica et Biophysica Acta (BBA)-Molecular Cell Research
- 出版年：2016
- 出版时间：April 2016
- 年：2016
- 卷：1863
- 期：4
- 页码：562-571
- 全文大小：1368 K
文摘
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Galectin inhibitor GCS-100 induces apoptosis in AML cells and synergizes with BH3 mimetics ABT-737 and ABT-199.
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GCS-100 suppresses ERK and AKT signaling, reduces MCL-1 protein expression, and induces p53 protein expression.
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Suppression of Galectin 3 supports MCL-1 gene and protein expression in wt p53 OCI-AML3 cells but not p53 null THP-1 cells.