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Decreased Lactate Dehydrogenase B Expression Triggers Mitochondrial Respiratory Defects and Delayed Cell Growth

Authors
Lee, Young-Kyoung; Kim, June-Hyung; Yoon, Gyesoon
Department
Department of Biochemistry & Molecular Biology
Abstract
Aerobic glycolysis (i.e. the Warburg effect) is a distinctive hallmark of solid tumors. We recently reported that increased glycolytic lactate production of hepatoma cells was linked with decreased lactate dehydrogenase (LDH) B expression and mitochondrial respiratory defects. In this study, we aimed to elucidate whether and how LDHB suppression contributes to mitochondrial dysfunction.

When we suppressed LDHB expression by siRNA-mediated knockdown, we clearly observed

decreased cellular oxygen consumption rate and delayed cell growth. Unexpectedly, we observed that in the hepatoma cells with low level of LDHB, such as SNU354 and SNU423, LDHA was not only located in cytoplasm but also in nucleus and mitochondria. LDHA translocation into mitochondria and nucleus was also observed by siRNA-mediated LDHB knockdown, implying that LDHA translocation may be associated with mitochondrial dysfunction. Taken together, our results

suggest that aerobic glycolysis and mitochondrial dysfunction, key metabolic signatures of cancer cell, can be triggered or maintained by suppressing LDHB during tumorigenesis.
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