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mTOR Signaling and Cancer Progression

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

cAMP-dependent Protein Kinase Pathways

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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...

Positive Regulator Molecules

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.

Positive Regulator Molecules

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.

M-Cdk Drives Transition Into Mitosis

M-Cdk Drives Transition Into Mitosis

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Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...

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Related Experiment Video

Updated: Apr 6, 2026

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method

Published on: October 23, 2018

c-Myc and AMPK Control Cellular Energy Levels by Cooperatively Regulating Mitochondrial Structure and Function.

Lia R Edmunds¹, Lokendra Sharma², Huabo Wang²

¹Section of Hematology/Oncology, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA, United States of America; The University of Pittsburgh School of Medicine, Pittsburgh, PA, United States of America.

|August 1, 2015

Summary

This summary is machine-generated.

The oncogene Myc and AMP-activated protein kinase (AMPK) are co-dependent, influencing cellular energy production. Their cross-talk impacts glycolysis and oxidative phosphorylation, crucial for ATP generation.

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Area of Science:

Cellular Metabolism
Oncogenesis
Mitochondrial Function

Background:

The c-Myc (Myc) oncoprotein and AMP-activated protein kinase (AMPK) are key regulators of cellular energy metabolism, controlling glycolysis and oxidative phosphorylation (Oxphos).
Myc overexpression can lead to ATP depletion, activating AMPK, suggesting a potential interplay between these pathways.

Purpose of the Study:

To investigate the co-dependency and cross-talk between Myc and AMPK in regulating cellular metabolism.
To compare the metabolic consequences of acute Myc induction in wild-type (WT) and AMPK-deficient (KO) murine embryo fibroblasts (MEFs).

Main Methods:

Comparison of metabolic profiles (glycolysis, Oxphos, mitochondrial mass, ROS production) in WT and KO MEFs following Myc-estrogen receptor (MycER) activation.
Analysis of electron transport chain function, TCA cycle intermediates, redox states, and transcriptional changes.
Unbiased mass spectrometry-based proteomic survey of mitochondrial proteins and enzyme activity assays.

Main Results:

AMPK-deficient MEFs exhibited higher basal glycolysis but a reduced capacity for increased Oxphos, mitochondrial mass, and ROS production upon MycER activation.
Significant differences in electron transport chain function, TCA cycle enzyme levels, and redox states were observed between WT and KO MEFs.
Mass spectrometry revealed ~15% of quantified mitochondrial proteins to be dependent on either AMPK or Myc, or both, impacting key metabolic enzymes like pyruvate kinase and pyruvate dehydrogenase.

Conclusions:

Myc and AMPK exhibit significant co-dependency and cross-talk in regulating metabolic pathways essential for ATP generation.
This interplay influences glycolysis, oxidative phosphorylation, and mitochondrial function, highlighting a complex regulatory network in cellular energy homeostasis.