Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.8K
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...
4.8K
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

4.3K
4.3K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

5.1K
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...
5.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.6K
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
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

10.1K
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...
10.1K
The Ras Gene02:38

The Ras Gene

5.7K
The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
5.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

KRAS Inhibitor Induced Cancer Cell Death Enhances Sensitivity to Immune-Mediated Bystander Killing of Drug-Resistant Subclones.

Cancer research·2026
Same author

Sensitizing Lung Cancer to Immunotherapy with a RAS(ON) Inhibitor Doublet.

Cancer discovery·2026
Same author

Nociceptive innervation limits tertiary lymphoid structures to promote lung cancer.

Cell·2026
Same author

A Roadmap to Transform Lung Cancer Outcomes: Priorities in Biology, Therapeutic Innovation, Early Detection, Prevention, and Interception.

Cancer discovery·2026
Same author

Retraction Note: Antibodies against endogenous retroviruses promote lung cancer immunotherapy.

Nature·2026
Same author

Covalent inhibitors of the PI3Kα RAS binding domain impair tumor growth driven by RAS and HER2.

Science (New York, N.Y.)·2025

Related Experiment Video

Updated: Apr 26, 2026

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.3K

Inhibiting the RAS-PI3K pathway in cancer therapy.

Clare Sheridan1, Julian Downward2

  • 1Signal Transduction Laboratory, Cancer Research UK London Research Institute, London, United Kingdom.

The Enzymes
|July 19, 2014
PubMed
Summary

The phosphoinositide 3-kinase (PI3K) pathway is frequently over-activated in cancers, driving tumor growth and survival. PI3K inhibitors are being investigated in clinical trials for cancer treatment, showing promising results and tolerable toxicity.

Keywords:
AKTCancerPI3KPI3K inhibitorsRasmTOR

More Related Videos

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

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

Published on: July 21, 2018

18.9K

Related Experiment Videos

Last Updated: Apr 26, 2026

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.3K
Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

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

Published on: July 21, 2018

18.9K

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • The phosphoinositide 3-kinase (PI3K) pathway is a critical regulator of cell growth, survival, and metabolism.
  • Over-activation of the PI3K pathway, through various genetic alterations, is a common event in human cancers.
  • This pathway's role in promoting tumor progression, including migration, invasion, and angiogenesis, makes it a key therapeutic target.

Purpose of the Study:

  • To review PI3K inhibitors currently under investigation for cancer treatment.
  • To discuss the opportunities and challenges identified in recent preclinical and clinical studies of PI3K pathway inhibition.

Main Methods:

  • Review of PI3K inhibitors in preclinical and clinical development.
  • Analysis of clinical trial data regarding efficacy and toxicity profiles.
  • Discussion of combination treatment strategies.

Main Results:

  • PI3K pathway inhibition is being actively explored in clinical trials for various cancers.
  • Initial clinical trial results indicate tolerable toxicity profiles for PI3K inhibitors.
  • Single-agent PI3K inhibitors have shown some benefit in advanced solid tumors.

Conclusions:

  • PI3K pathway inhibitors represent a promising therapeutic strategy for cancer treatment.
  • Combination therapies involving PI3K inhibitors may offer enhanced anti-cancer effects.
  • Further investigation is needed to overcome obstacles and optimize the use of PI3K inhibitors in oncology.