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

Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Activation of Integrins01:15

Activation of Integrins

Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding events provide an effective stimulus.
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

You might also read

Related Articles

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

Sort by
Same author

Cell painting and thermal proteome profiling for inference of drug targets and mechanism of action.

Molecular systems biology·2026
Same author

Towards a novel toxicity prediction pipeline, combining PBPK models and mechanistic cellular adversity models.

Toxicology·2026
Same author

Pulling the strings: Contractile VE-cadherin junctions to stabilize angiogenic sprouts.

The Journal of cell biology·2026
Same author

VE-cadherin interaction proteomics identifies ARVCF as stabilizer of endothelial adherens junctions.

iScience·2026
Same author

Stakeholder input towards further refinement and consolidation of the alternative safety profiling algorithm (ASPA) for next generation risk assessment (NGRA).

ALTEX·2026
Same author

ReCHEMbinant stapling enhances intracellular delivery and bioactivity of engineered protein inhibitors.

Chem·2026

Related Experiment Video

Updated: Jun 26, 2026

Measurement of Cellular Chemotaxis with ECIS/Taxis
11:37

Measurement of Cellular Chemotaxis with ECIS/Taxis

Published on: April 1, 2012

Cross-talk between integrins and oncogenes modulates chemosensitivity.

Jordi Carreras Puigvert1, Stephan Huveneers, Lisa Fredriksson

  • 1Division of Toxicology, Leiden Amsterdam Center for Drug Research, Leiden University, Leiden, The Netherlands.

Molecular Pharmacology
|January 23, 2009
PubMed
Summary

Cancer treatment efficacy depends on oncogene and integrin expression. Certain oncogenes like c-Src, combined with specific integrins (beta1), enhance chemotherapy"s cancer cell-killing effects by increasing stress and caspase activation.

More Related Videos

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line
06:24

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line

Published on: April 11, 2025

A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion
06:36

A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion

Published on: April 24, 2015

Related Experiment Videos

Last Updated: Jun 26, 2026

Measurement of Cellular Chemotaxis with ECIS/Taxis
11:37

Measurement of Cellular Chemotaxis with ECIS/Taxis

Published on: April 1, 2012

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line
06:24

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line

Published on: April 11, 2025

A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion
06:36

A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion

Published on: April 24, 2015

Area of Science:

  • Molecular oncology and cancer cell biology
  • Integrin signaling and cancer therapeutics

Background:

  • Chemotherapy effectiveness often hinges on inducing cancer cell death via DNA damage.
  • The p53 tumor suppressor pathway, crucial for DNA damage response, is frequently lost in cancer.
  • Cancer cell sensitivity to genotoxic agents is influenced by oncogenic signaling and microenvironment interactions.

Purpose of the Study:

  • To investigate how oncogenes modulate cellular responses to genotoxic agents.
  • To examine the role of integrin adhesion receptors in mediating chemoresistance or sensitization.
  • To understand the interplay between specific oncogenes (c-Src, H-Ras) and integrins (beta1, beta3) in cancer cell death pathways.

Main Methods:

  • Utilized epithelial cells with suppressed p53 activity expressing either beta1 or beta3 integrins.
  • Treated cells with genotoxic agents like cisplatin.
  • Assessed apoptosis, G(2) arrest, endoplasmic reticulum stress, and caspase-3 activation in response to oncogene and integrin expression profiles.

Main Results:

  • Cells expressing beta1 integrins and the c-Src[Y530F] oncogene showed enhanced apoptosis upon genotoxic treatment.
  • This sensitization was reduced in cells expressing beta3 integrins instead of beta1.
  • The H-Ras[G12V] oncogene did not sensitize cells to genotoxicants, irrespective of integrin type.
  • c-Src[Y530F]-mediated sensitization involved endoplasmic reticulum stress and caspase-3 activation, independent of p53.

Conclusions:

  • Oncogene and integrin expression profiles significantly impact cancer cell response to genotoxic chemotherapy.
  • The c-Src oncogene, in conjunction with beta1 integrins, can sensitize cancer cells to chemotherapy through non-p53 pathways.
  • These findings suggest that targeting oncogene-integrin interactions could be a strategy to improve chemotherapy efficacy.