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Related Concept Videos

mTOR Signaling and Cancer Progression03:03

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...
mTOR Signaling and Cancer Progression03:03

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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...
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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 rapamycin-insensitive companion...
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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Targeted Cancer Therapies02:57

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Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
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Cancer therapy: staying current with AMPK.

David A Fruman1, Aimee L Edinger

  • 1Department of Molecular Biology and Biochemistry, University of California Irvine, Irvine, CA 92697, USA. dfruman@uci.edu

The Biochemical Journal
|May 10, 2008
PubMed
Summary

The LKB1-AMPK pathway

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • The role of the LKB1-AMPK pathway in cancer is debated, with theories suggesting it either suppresses tumor formation or aids cancer cell survival.
  • PTEN loss is a common event in human cancers, often leading to uncontrolled cell growth.

Purpose of the Study:

  • To investigate whether the LKB1-AMPK pathway suppresses tumorigenesis or rescues cancer cells from metabolic stress.
  • To determine the effect of AMPK activators on tumor growth in a relevant preclinical model.

Main Methods:

  • Utilized a mouse model with spontaneous tumors due to heterozygous PTEN deficiency.
  • Administered AMPK activators to assess their impact on tumor growth dynamics.

Main Results:

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  • AMPK activators were found to significantly delay the growth of spontaneous tumors in PTEN-deficient mice.
  • This suggests a tumor-suppressive role for the LKB1-AMPK pathway in this context.

Conclusions:

  • The LKB1-AMPK pathway acts to suppress tumorigenesis.
  • Activating AMPK can be a potential therapeutic strategy to control tumor progression in PTEN-deficient cancers.