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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

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...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...

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Related Experiment Video

Updated: Jun 30, 2026

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration
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Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration

Published on: June 9, 2023

Metastasis and AKT activation.

Meng Qiao1, Shijie Sheng, Arthur B Pardee

  • 1Dana-Farber Cancer Institute, Boston, Massachusetts, USA. meng_qiao@dfci.harvard.edu

Cell Cycle (Georgetown, Tex.)
|September 27, 2008
PubMed
Summary
This summary is machine-generated.

The activated AKT pathway drives cancer metastasis by promoting cell escape and growth. Understanding AKT

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Metastasis is a critical factor in 90% of cancer-related deaths, necessitating research into its molecular mechanisms for improved detection and treatment.
  • The activated AKT kinase plays a crucial role in multiple metastatic processes, including cellular detachment, proliferation, apoptosis evasion, and angiogenesis.
  • Activation of AKT, often through phosphorylation at Ser-473, initiates a cascade of events critical for the development of metastatic properties.

Purpose of the Study:

  • To investigate the molecular connections between AKT activation and the metastatic cascade.
  • To elucidate the mechanisms by which AKT becomes hyperactivated in metastatic cancer cells.
  • To identify potential therapeutic targets within the AKT signaling pathway.

Main Methods:

  • Analysis of the AKT signaling pathway and its downstream targets.
  • Investigation of factors influencing AKT activation, including PI3K, TORC2, PHLPP, and PTEN.
  • Examination of the role of SNAIL and E-cadherin in AKT-mediated metastasis.

Main Results:

  • Activated AKT phosphorylates GSK-3beta, leading to its degradation and increased stability of the transcription factor SNAIL.
  • Decreased E-cadherin transcription, resulting from SNAIL stabilization, reduces cell-cell adhesion and facilitates cellular detachment.
  • Potential mechanisms for AKT hyperactivation include increased PI3K or TORC2 activity, or decreased PHLPP phosphatase activity.
  • A positive feedback loop involving decreased E-cadherin, reduced PTEN, and increased PIP3 further enhances AKT activation and promotes metastasis.

Conclusions:

  • The activated AKT pathway is a central regulator of cancer metastasis through its effects on cell adhesion, proliferation, and survival.
  • Dysregulation of key components in the PI3K/AKT pathway, such as PI3K, TORC2, PHLPP, and PTEN, contributes to AKT hyperactivation in metastatic cells.
  • Targeting the AKT signaling pathway and its downstream effectors represents a promising strategy for the development of novel anti-metastatic therapies.