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

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.5K
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...
7.5K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

3.3K
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.3K
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

3.9K
Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
3.9K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.7K
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...
3.7K
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

4.9K
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
4.9K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

2.1K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.1K

You might also read

Related Articles

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

Sort by
Same author

Intranasal Trans-Sialidase Vaccine Mitigates Acute and Chronic Pathology in a Preclinical Oral Chagas Disease Model.

Vaccines·2024
Same author

Synthesis of Structurally Related Coumarin Derivatives as Antiproliferative Agents.

ACS omega·2023
Same author

Synuclein Proteins in Cancer Development and Progression.

Biomolecules·2023
Same author

Allergic Sensitization Driving Immune Phenotyping and Disease Severity in a Mouse Model of Asthma.

Allergy, asthma & immunology research·2023
Same author

Rac1 as a Target to Treat Dysfunctions and Cancer of the Bladder.

Biomedicines·2022
Same author

The Endothelial Dysfunction Could Be a Cause of Heart Failure with Preserved Ejection Fraction Development in a Rat Model.

Oxidative medicine and cellular longevity·2022

Related Experiment Video

Updated: Jun 8, 2025

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

13.6K

Overcoming Therapy Resistance in Colorectal Cancer: Targeting the Rac1 Signaling Pathway as a Potential Therapeutic

Luciano E Anselmino1,2,3,4, Florencia Malizia1,2,3,4, Aylén Avila3,4

  • 1Instituto de Inmunología Clínica y Experimental de Rosario (IDICER, CONICET-UNR), Facultad de Ciencias Médicas (UNR), Rosario 2000, Argentina.

Cells
|November 8, 2024
PubMed
Summary
This summary is machine-generated.

Colorectal cancer (CRC) patients resistant to 5-fluorouracil (5-FU) chemotherapy may benefit from targeting Rac1. A novel Rac1 inhibitor, 1A-116, restored 5-FU sensitivity and inhibited tumor growth and metastasis in preclinical models.

Keywords:
Rac1colorectal cancerrepositioningresistancesmall GTPases

More Related Videos

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

7.2K
Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer
06:19

Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer

Published on: July 18, 2017

9.9K

Related Experiment Videos

Last Updated: Jun 8, 2025

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

13.6K
Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

7.2K
Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer
06:19

Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer

Published on: July 18, 2017

9.9K

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide.
  • 5-fluorouracil (5-FU) is a cornerstone chemotherapy for CRC, but resistance is a significant clinical challenge.
  • Understanding mechanisms of 5-FU resistance is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To elucidate molecular mechanisms underlying CRC resistance and recurrence following 5-FU treatment.
  • To identify novel therapeutic targets and agents to overcome 5-FU resistance in CRC.

Main Methods:

  • Integrated in silico, in vitro, and in vivo approaches to study 5-FU resistance.
  • Bioinformatic analysis to identify differentially expressed genes and enriched pathways.
  • Drug screening to identify agents that restore 5-FU sensitivity.
  • Preclinical evaluation of a novel Rac1 inhibitor (1A-116) in 5-FU resistant CRC models.

Main Results:

  • Identified key genes and pathways associated with 5-FU resistance and recurrence.
  • Discovered that the Rac1 inhibitor 1A-116 reversed 5-FU resistance phenotypes in vitro.
  • Demonstrated that 1A-116 inhibited tumor growth and metastasis in vivo.
  • Confirmed restoration of 5-FU sensitivity in resistant cells upon 1A-116 treatment.

Conclusions:

  • Targeting Rac1, a key regulator of cellular processes, is a promising strategy to overcome 5-FU resistance in CRC.
  • The novel Rac1 inhibitor 1A-116 shows potential as a therapeutic agent for 5-FU resistant colorectal cancer.
  • Further investigation into Rac1 inhibition could lead to improved treatment outcomes for CRC patients.