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Updated: Apr 29, 2026

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines
Published on: March 17, 2023
mTORC2 in the center of cancer metabolic reprogramming
Kenta Masui1, Webster K Cavenee2, Paul S Mischel2
1Ludwig Institute for Cancer Research, University of California San Diego, La Jolla, CA 92093, USA; Laboratory of Neuropathology, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan.
Abstract:
Metabolic reprogramming is a central hallmark of cancer, enabling tumor cells to obtain the macromolecular precursors and energy needed for rapid tumor growth. Understanding how oncogenes coordinate altered signaling with metabolic reprogramming and global transcription may yield new insights into tumor pathogenesis, and provide a new landscape of promising drug targets, while yielding important clues into mechanisms of resistance to the signal transduction inhibitors currently in use. We review here the recently identified central regulatory role for mechanistic target of rapamycin complex 2 (mTORC2), a downstream effector of many cancer-causing mutations, in metabolic reprogramming and cancer drug resistance. We consider the impact of mTORC2-related metabolism on epigenetics and therapeutics, with a particular focus on the intractable malignant brain tumor, glioblastoma multiforme (GBM).
Insights
Cancer cells reprogram metabolism for growth, and mechanistic target of rapamycin complex 2 (mTORC2) is key. This review explores mTORC2
Area of Science:
- Oncology
- Molecular Biology
- Cancer Metabolism
Background:
- Metabolic reprogramming is a hallmark of cancer, fueling tumor growth.
- Oncogenes drive altered signaling, metabolism, and transcription in cancer.
- Understanding these links offers new therapeutic targets and insights into drug resistance.
Purpose of the Study:
- To review the central regulatory role of mechanistic target of rapamycin complex 2 (mTORC2) in cancer.
- To explore mTORC2's impact on metabolic reprogramming and drug resistance.
- To focus on mTORC2's role in glioblastoma multiforme (GBM) therapeutics.
Main Methods:
- Literature review of recent findings on mTORC2.
- Analysis of mTORC2's downstream effects on cellular metabolism.
- Examination of mTORC2's influence on epigenetic modifications and therapeutic resistance.
Main Results:
- mTORC2 plays a critical role in coordinating cancer cell metabolism.
- mTORC2 signaling impacts epigenetic regulation and therapeutic outcomes.
- mTORC2 is implicated in resistance to signal transduction inhibitors.
Conclusions:
- mTORC2 is a pivotal regulator of cancer metabolism and drug resistance.
- Targeting mTORC2 offers a promising therapeutic strategy, especially for glioblastoma.
- Further research into mTORC2-driven metabolism is crucial for advancing cancer treatment.
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