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A novel miR-155/miR-143 cascade controls glycolysis by regulating hexokinase 2 in breast cancer cells
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A novel miR-155/miR-143 cascade controls glycolysis by regulating hexokinase 2 in breast cancer cells
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A novel miR-155/miR-143 cascade controls glycolysis by regulating hexokinase 2 in breast cancer cells
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Journal Article
A novel miR-155/miR-143 cascade controls glycolysis by regulating hexokinase 2 in breast cancer cells
2012
Overview
Cancer cells preferentially metabolize glucose through aerobic glycolysis. This phenomenon, known as the Warburg effect, is an anomalous characteristic of glucose metabolism in cancer cells. Chronic inflammation is a key promoting factor of tumourigenesis. It remains, however, largely unexplored whether and how pro‐tumourigenic inflammation regulates glucose metabolism in cancer cells. Here, we show that pro‐inflammatory cytokines promote glycolysis in breast cancer cells, and that the inflammation‐induced miR‐155 functions as an important mediator in this process. We further show that miR‐155 acts to upregulate
hexokinase 2
(
hk2
), through two distinct mechanisms. First, miR‐155 promotes
hk2
transcription by activation of signal transducer and activator of transcription 3 (STAT3), a transcriptional activator for
hk2
. Second, via targeting
C
/
EBP
β (a transcriptional activator for
mir‐143
), miR‐155 represses
mir‐143
, a negative regulator of
hk2
, thus resulting in upregulation of
hk2
expression at the post‐transcriptional level. The miR‐155‐mediated
hk2
upregulation also appears to operate in other types of cancer cells examined. We suggest that the miR‐155/miR‐143/HK2 axis may represent a common mechanism linking inflammation to the altered metabolism in cancer cells.
Molecular analyses in this study identify inflammation‐induced miRNA regulation of central glycolytic enzymes. Focussing on hexokinase‐2 as major target therapeutically exploitable consequences for cell proliferation, migration, and metastasis are functionally established.
