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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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.
There are several types of targeted therapies against specific...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
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...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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...

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Related Experiment Video

Updated: Jun 2, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
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Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

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Targeting PDK1 in cancer.

C Raimondi1, M Falasca

  • 1Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute of Cell and Molecular Science, Centre for Diabetes, Inositide Signalling Group, London E1 2AT, UK. m.falasca@qmul.ac.uk

Current Medicinal Chemistry
|May 17, 2011
PubMed
Summary

Phosphoinositide 3-kinase (PI3K) pathway activation drives cancer. 3-phosphoinositide-dependent protein kinase 1 (PDK1) is crucial for this pathway, making PDK1 inhibitors a potential therapeutic strategy for cancer treatment.

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Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
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Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
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Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Aberrant phosphoinositide 3-kinase (PI3K) signaling is a hallmark of many cancers, disrupting cell survival, growth, proliferation, and migration.
  • Mutations in the tumor suppressor PTEN frequently lead to uncontrolled PI3K pathway activation, contributing to oncogenesis.
  • 3-phosphoinositide-dependent protein kinase 1 (PDK1) and protein kinase B (PKB)/Akt are key downstream effectors of PI3K, playing critical roles in various cancer types.

Purpose of the Study:

  • To review the role of PDK1 in cancer progression, particularly in the context of PI3K pathway activation.
  • To explore the potential of PDK1 as a therapeutic target for cancer treatment.
  • To discuss current approaches for inhibiting PDK1 activity.

Main Methods:

  • Literature review of published data on PDK1 function in cancer.
  • Analysis of studies investigating the link between PDK1, PI3K signaling, and cancer cell behavior.
  • Examination of evidence supporting PDK1 as a therapeutic target.

Main Results:

  • Alterations in PDK1 are integral to oncogenic PI3K signaling, especially in breast cancer.
  • PDK1 is essential for regulating cancer cell migration and metastasis, particularly when PTEN is deficient.
  • Downregulation of PDK1 inhibits the migration and experimental metastasis of human breast cancer cells.
  • PDK1 activates numerous proteins, including Akt, PKC isoforms, S6K, and SGK, and is oncogenic in a PI3K-dependent manner.

Conclusions:

  • PDK1 is a critical mediator of PI3K pathway-driven oncogenesis and cancer cell dissemination.
  • PDK1 represents a promising therapeutic target for inhibiting cancer progression and metastasis.
  • PDK1 inhibitors hold potential for clinical application in cancer therapy.