Akt stimulates aerobic glycolysis in cancer cells (VSports注册入口)
- PMID: 15172999
- DOI: V体育官网 - 10.1158/0008-5472.CAN-03-2904
"VSports app下载" Akt stimulates aerobic glycolysis in cancer cells
Abstract
Cancer cells frequently display high rates of aerobic glycolysis in comparison to their nontransformed counterparts, although the molecular basis of this phenomenon remains poorly understood. Constitutive activity of the serine/threonine kinase Akt is a common perturbation observed in malignant cells. Surprisingly, although Akt activity is sufficient to promote leukemogenesis in nontransformed hematopoietic precursors and maintenance of Akt activity was required for rapid disease progression, the expression of activated Akt did not increase the proliferation of the premalignant or malignant cells in culture. However, Akt stimulated glucose consumption in transformed cells without affecting the rate of oxidative phosphorylation. High rates of aerobic glycolysis were also identified in human glioblastoma cells possessing but not those lacking constitutive Akt activity. Akt-expressing cells were more susceptible than control cells to death after glucose withdrawal VSports手机版. These data suggest that activation of the Akt oncogene is sufficient to stimulate the switch to aerobic glycolysis characteristic of cancer cells and that Akt activity renders cancer cells dependent on aerobic glycolysis for continued growth and survival. .
Comment in
-
"V体育官网" Cancer Signaling Drives Cancer Metabolism: AKT and the Warburg Effect.Cancer Res. 2021 Oct 1;81(19):4896-4898. doi: 10.1158/0008-5472.CAN-21-2647. Cancer Res. 2021. PMID: 34598998
Publication types
- "V体育2025版" Actions
MeSH terms
- Actions (VSports最新版本)
- VSports注册入口 - Actions
- VSports在线直播 - Actions
- VSports app下载 - Actions
- "VSports" Actions
- VSports app下载 - Actions
- V体育官网入口 - Actions
- "VSports注册入口" Actions
- Actions (V体育ios版)
V体育2025版 - Substances
- "VSports注册入口" Actions
- V体育官网入口 - Actions
"V体育平台登录" Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical (V体育2025版)
Miscellaneous
