Related Experiment Video

Updated: May 7, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

960

New connections between old pathways: PDK1 signaling promotes cellular transformation through PLK1-dependent MYC

John T Cunningham1, Davide Ruggero

  • 1Department of Urology, School of Medicine, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California.

Cancer Discovery
|October 15, 2013
PubMed

Insights

Researchers discovered a new signaling pathway (PDK1-PLK1-MYC) linking key cancer-driving programs. Inhibiting this pathway offers a promising therapeutic strategy for difficult-to-treat cancers, particularly those with high MYC levels.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling Networks

Background:

  • Understanding the interplay between oncogenic pathways is crucial for developing effective cancer therapies.
  • Malignancies often involve complex networks of driver oncogenic signals, posing therapeutic challenges.

Discussion:

  • Tan and colleagues identify a novel PDK1-PLK1-MYC signaling axis.
  • This pathway connects the phosphoinositide 3-kinase (PI3K) and MYC oncogenic programs.
  • The study elucidates the functional role of this signaling in cancer cell survival and tumorigenesis.

Key Insights:

  • The PDK1-PLK1-MYC pathway is critical for cancer cell survival and tumor formation.
  • Pharmacological inhibition of PDK1 and PLK1 demonstrates therapeutic benefits in preclinical cancer models.
  • Targeting this pathway is effective against cancers with high MYC oncoprotein levels, often considered 'undruggable'.

Outlook:

  • This discovery opens new avenues for targeted cancer therapies.
  • Inhibition of the PDK1-PLK1-MYC axis represents a potential strategy for overcoming therapeutic resistance.
  • Further research may explore combination therapies targeting this pathway in various MYC-driven cancers.

More Related Videos

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

18.3K
Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development09:32

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development

Published on: June 15, 2017

8.0K

Related Concept Videos

Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
4.7K
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...
5.2K
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...
5.4K
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

2.5K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.0K
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...
3.6K