Autophagy is an important metabolic pathway to determine leukemia cell survival following suppression of the glycolytic pathway.
Most cancer cells predominantly produce energy by glycolysis, even in the presence of adequate oxygen. Therefore, inhibition of glycolysis is a promising cancer treatment target. Recently, it has been recognized that to conduct thorough treatment of cancer, comprehensive understanding of cancer metabolism is essential, not only focusing on glycolysis. Here, we investigated the supporting mechanism of autophagy, which is a catabolic process that recycles intracellular components, for energy supply in the glycolysis-inhibited condition. Autophagy is thought to be highly activated in cancers and to promote their growth or progression by adapting to the harsh surrounding microenvironment. We found that cancer cells positively promoted autophagy to overcome the energy shortage from glycolysis by maintaining mitochondrial activity for ATP production essential for survival. Conclusively, autophagy plays a role in determining whether cancer cells live or die, and autophagic ability in cancer cells is a promising target for therapy.
Laboratory of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-shi, Chiba 260-8675, Japan.
Moemi
M
Kawaguchi
Laboratory of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-shi, Chiba 260-8675, Japan. Electronic address: aokishigeki@chiba-u.jp.
Shigeki
S
Aoki
Laboratory of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-shi, Chiba 260-8675, Japan.
Takuya
T
Hirao
Laboratory of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-shi, Chiba 260-8675, Japan.
Michie
M
Morita
Laboratory of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-shi, Chiba 260-8675, Japan.
Kousei
K
Ito
D001343:Autophagy; D002470:Cell Survival; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism*; D006019:Glycolysis; D006801:Humans; D019169:Jurkat Cells; D007938:Leukemia / Q000378:metabolism* / Q000473:pathology*; D008928:Mitochondria / Q000378:metabolism
D005947:Glucose
Autophagy; Cancer energy metabolism; Glycolysis; Leukemia cells; Oxidative phosphorylation; Pentose phosphate pathway