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Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

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 rapamycin-insensitive companion...
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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Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...

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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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PI3K/AKT/mTOR Pathway in Angiogenesis.

Jayashree Karar1, Amit Maity

  • 1Department of Radiation Oncology, Perelman School of Medicine at the University of Pennsylvania Philadelphia, PA, USA.

Frontiers in Molecular Neuroscience
|December 7, 2011
PubMed
Summary
This summary is machine-generated.

The phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway is crucial for cancer growth and angiogenesis. Inhibiting this pathway can impact tumor vascularization, with potential for both normalization and adverse effects.

Keywords:
PI3K/AKT/mTORVEGFangiogenesisangiopoietinsnitric oxide

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Area of Science:

  • Oncology
  • Molecular Biology
  • Vascular Biology

Background:

  • The PI3K/AKT/mTOR pathway is frequently activated in human cancers, regulating key cellular functions.
  • This pathway is implicated in tumor progression, including proliferation, survival, and metastasis.
  • Its role in angiogenesis, the formation of new blood vessels, is critical for tumor growth.

Purpose of the Study:

  • To review the role of the PI3K/AKT/mTOR pathway in angiogenesis within the context of cancer.
  • To explore the mechanisms by which this pathway influences the production of angiogenic factors like VEGF.
  • To discuss the therapeutic implications of targeting the PI3K/AKT/mTOR pathway in cancer treatment.

Main Methods:

  • Review of existing literature on the PI3K/AKT/mTOR pathway and its involvement in angiogenesis.
  • Analysis of studies investigating the connection between PI3K activation and vascular endothelial growth factor (VEGF) production.
  • Examination of preclinical and clinical data on PI3K/AKT/mTOR inhibitors and their effects on tumor vasculature.

Main Results:

  • PI3K/AKT/mTOR pathway activation promotes angiogenesis through various mechanisms, including increased VEGF secretion.
  • Hypoxia-inducible factor 1 (HIF-1) and other factors mediate the pathway's influence on VEGF.
  • Inhibitors of the PI3K/AKT/mTOR pathway can reduce VEGF levels and impact tumor vasculature, sometimes leading to normalization.
  • The pathway is also essential for normal blood vessel development and endothelial cell function.

Conclusions:

  • The PI3K/AKT/mTOR pathway is a significant regulator of angiogenesis in both cancer and normal development.
  • Targeting this pathway offers therapeutic potential but requires careful consideration of its complex effects on tumor vasculature.
  • Understanding the interplay between PI3K signaling and angiogenic factors is crucial for effective cancer therapy.