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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adult, Antibiotics, Antineoplastic, Bone Marrow Cells, Cell Line, Tumor, Doxorubicin, Drug Resistance, Neoplasm, Female, Fluorouracil, Glucose, Glucose Transporter Type 1, HL-60 Cells, Humans, Hypoxia-Inducible Factor 1, alpha Subunit, Leukemia, Myeloid, Acute, Leukocytes, Mononuclear, Male, Middle Aged, RNA Interference, RNA, Messenger, RNA, Small Interfering, Young Adult.
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Is hIF-1α and GLUT1 gene expression associated with chemoresistance of acute myeloid leukemia? Context: 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). 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). 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.
assistant
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. Final Decision: yes