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

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.8K
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...
3.8K
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
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

3.7K
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...
3.7K

You might also read

Related Articles

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

Sort by
Same author

Axially Swept Light-Sheet Microscopy using scattering and fluorescence contrast mechanisms.

Proceedings of SPIE--the International Society for Optical Engineering·2026
Same author

Label-Free and High-Throughput Quantification of Nanoparticle-Cell Interactions at the Single-Cell Level with Flow Cytometry.

Analytical chemistry·2026
Same author

Promoting Self-Efficacy of Biomedical Engineering Undergraduate Students Using a Deliberately Designed Nanomedicine Workshop Series.

Biomedical engineering education·2026
Same author

YES Oklahoma: Building Pathways into Cancer Research and Public Health for Indigenous High School Students.

Journal of cancer education : the official journal of the American Association for Cancer Education·2026
Same author

Lipid Nanoparticle Surface Engineering with Heparosan Polysaccharides for Safe and Effective mRNA Delivery <i>In Vitro</i> and <i>In Vivo</i>.

ACS applied materials & interfaces·2026
Same author

Epidemiology, treatment patterns, and survival outcomes of patients with mantle cell lymphoma in Germany: a retrospective analysis of administrative claims data.

Annals of hematology·2026

Related Experiment Video

Updated: Jul 31, 2025

Automated Imaging and Analysis for the Quantification of Fluorescently Labeled Macropinosomes
11:01

Automated Imaging and Analysis for the Quantification of Fluorescently Labeled Macropinosomes

Published on: August 24, 2021

2.8K

Gold Nanoparticles Inhibit Macropinocytosis by Decreasing KRAS Activation.

Chandra Kumar Elechalawar1, Geeta Rao1, Suresh Kumar Gulla1

  • 1Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, United States.

ACS Nano
|May 2, 2023
PubMed
Summary
This summary is machine-generated.

Gold nanoparticles (GNP) inhibit cancer cell growth by blocking KRAS activation and macropinocytosis. Unmodified GNP effectively targets KRAS, offering a new strategy against RAS-driven tumors.

Keywords:
KRASRASgold nanoparticlesmacropinocytosispancreatic ductal adenocarcinoma

More Related Videos

Protein Kinase C-delta Inhibitor Peptide Formulation using Gold Nanoparticles
06:06

Protein Kinase C-delta Inhibitor Peptide Formulation using Gold Nanoparticles

Published on: March 9, 2019

5.5K
Preparation and Photoacoustic Analysis of Cellular Vehicles Containing Gold Nanorods
10:46

Preparation and Photoacoustic Analysis of Cellular Vehicles Containing Gold Nanorods

Published on: May 2, 2016

6.9K

Related Experiment Videos

Last Updated: Jul 31, 2025

Automated Imaging and Analysis for the Quantification of Fluorescently Labeled Macropinosomes
11:01

Automated Imaging and Analysis for the Quantification of Fluorescently Labeled Macropinosomes

Published on: August 24, 2021

2.8K
Protein Kinase C-delta Inhibitor Peptide Formulation using Gold Nanoparticles
06:06

Protein Kinase C-delta Inhibitor Peptide Formulation using Gold Nanoparticles

Published on: March 9, 2019

5.5K
Preparation and Photoacoustic Analysis of Cellular Vehicles Containing Gold Nanorods
10:46

Preparation and Photoacoustic Analysis of Cellular Vehicles Containing Gold Nanorods

Published on: May 2, 2016

6.9K

Area of Science:

  • Oncology
  • Nanotechnology
  • Molecular Biology

Background:

  • RAS-transformed cells rely on macropinocytosis for amino acid uptake to fuel uncontrolled proliferation.
  • Targeting RAS to inhibit macropinocytosis presents a significant therapeutic challenge in cancer treatment.

Purpose of the Study:

  • To investigate the potential of gold nanoparticles (GNP) in inhibiting macropinocytosis by targeting KRAS activation.
  • To evaluate the efficacy of GNP in preclinical models of pancreatic cancer.

Main Methods:

  • Utilized surface-modified and unmodified GNP to assess their interaction with wild-type and mutant KRAS.
  • Measured KRAS activation, downstream signaling, macropinocytosis rates, and tumor cell growth in vitro.
  • Assessed the therapeutic effect of GNP in preclinical human xenograft models of pancreatic cancer in vivo.

Main Results:

  • Unmodified GNP specifically sequestered both wild-type and mutant KRAS, inhibiting its activation independently of growth factor stimulation.
  • Surface-passivated GNP demonstrated no significant effect on KRAS activation or macropinocytosis.
  • Inhibition of KRAS activation by GNP led to reduced macropinocytosis, decreased tumor cell growth in vitro, and suppressed tumor growth in vivo.

Conclusions:

  • Gold nanoparticles, particularly unmodified ones, can effectively inhibit macropinocytosis by decreasing KRAS activation.
  • This NP-mediated inhibition presents a promising translational strategy for targeting tumor growth in KRAS-driven cancers.