Literature DB >> 24641416

HIF-1α and GLUT1 gene expression is associated with chemoresistance of acute myeloid leukemia.

Kui Song1, Min Li, Xiao-Jun Xu, Li Xuan, Gui-Nian Huang, Xiao-Ling Song, Qi-Fa Liu.   

Abstract

AIMS: Much evidence suggests that increased glucose metabolism in tumor cells might contribute to the development of acquired chemoresistance. However, the molecular mechanisms are not fully clear. Therefore, we investigated a possible correlation of mRNA expression of HIF-1α and GLUT1 with chemoresistance in acute myeloid leukemia (AML).
METHODS: Bone marrow samples were obtained from newly diagnosed and relapsed AML (M3 exclusion) cases. RNA interference with short hairpin RNA (shRNA) was used to stably silence GLUT1 or HIF-1α gene expression in an AML cell line and HIF-1α and GLUT1 mRNA expression was measured by real-time quantitative polymerase chain reaction assay (qPCR).
RESULTS: High levels of HIF-1α and GLUT1 were associated with poor responsiveness to chemotherapy in AML. Down-regulation of the expression of GLUT1 by RNA interference obviously sensitized drug-resistant HL-60/ADR cells to adriamycin (ADR) in vitro, comparable with RNA interference for the HIF-1α gene.
CONCLUSIONS: Our data revealed that over-expression of HIF-1α and GLUT1 might play a role in the chemoresistance of AML. GLUT1 might be a potential target to reverse such drug resistance.

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Year:  2014        PMID: 24641416     DOI: 10.7314/apjcp.2014.15.4.1823

Source DB:  PubMed          Journal:  Asian Pac J Cancer Prev        ISSN: 1513-7368


  24 in total

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4.  Does aberrant membrane transport contribute to poor outcome in adult acute myeloid leukemia?

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Journal:  Front Pharmacol       Date:  2015-07-02       Impact factor: 5.810

5.  Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143.

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6.  Inhibiting autophagy targets human leukemic stem cells and hypoxic AML blasts by disrupting mitochondrial homeostasis.

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10.  ZnCl2 sustains the adriamycin-induced cell death inhibited by high glucose.

Authors:  A Garufi; D Trisciuoglio; M Cirone; G D'Orazi
Journal:  Cell Death Dis       Date:  2016-06-30       Impact factor: 8.469

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