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

Abnormal Proliferation02:23

Abnormal Proliferation

4.4K
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...
4.4K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.6K
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...
4.6K

You might also read

Related Articles

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

Sort by
Same author

[Hemodynamic effects of synchronous and asynchronous independent lung ventilation with different levels of positive end-expiratory pressure and tidal volumes on unilateral lung injury in dogs].

Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases·2010
Same author

[Study on the immuno-effects and influencing factors of Chinese hamster ovary (CHO) cell hepatitis B vaccine among adults, under different dosages].

Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi·2010
Same author

Assemblies of fluorine containing bent-shaped liquid crystal molecules studied by using scanning tunneling microscopy.

Journal of nanoscience and nanotechnology·2010
Same author

Carbon nanotubes induce secondary structure changes of bovine albumin in aqueous phase.

Journal of nanoscience and nanotechnology·2010
Same author

[Immunogenicity and protective efficacy of pertactin recombinants against Bordetella bronchiseptica challenge].

Wei sheng wu xue bao = Acta microbiologica Sinica·2010
Same author

[Analysis of the electrocardiographic findings in 288 patients with acute pulmonary thromboembolism].

Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases·2010

Related Experiment Video

Updated: May 13, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
04:01

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Published on: March 15, 2024

794

FADS2 inhibits colorectal cancer cell proliferation by regulating ferroptosis through SLC7A11/GPX4.

Qinghui Yang1,2, Hao Zhang1,2, Jing Luo1,2

  • 1Department of Oncology, Minhang Branch, Zhongshan Hospital, Fudan University, No. 170 Xinsong Road, Minhang District, Shanghai, China.

Molecular Biology Reports
|April 15, 2025
PubMed
Summary

Targeting FADS2 may inhibit colorectal cancer (CRC) progression by promoting ferroptosis. FADS2 knockdown suppresses CRC cell growth and enhances sensitivity to oxaliplatin chemotherapy.

Keywords:
FADS2Cell proliferationColorectal cancerFerroptosisPrognosis

More Related Videos

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
06:21

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer

Published on: May 10, 2024

594
Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

12.3K

Related Experiment Videos

Last Updated: May 13, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
04:01

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Published on: March 15, 2024

794
Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
06:21

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer

Published on: May 10, 2024

594
Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

12.3K

Area of Science:

  • Oncology
  • Cell Death Mechanisms
  • Molecular Biology

Background:

  • Colorectal cancer (CRC) remains a significant global health challenge, with high mortality rates.
  • Ferroptosis, a form of regulated cell death driven by lipid peroxidation, plays a critical role in cancer biology.
  • Understanding the molecular mechanisms underlying CRC progression, including the role of ferroptosis, is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the prognostic significance of FADS2 in colorectal cancer.
  • To elucidate the role of FADS2 in regulating ferroptosis within CRC cells.
  • To explore the therapeutic potential of targeting FADS2 for CRC treatment.

Main Methods:

  • Differential gene expression analysis of CRC datasets (TCGA-COAD, GSE36400) to identify key ferroptosis-related genes.
  • LASSO Cox regression for prognosis-associated gene identification and clinical significance evaluation of FADS2.
  • In vitro experiments assessing the impact of FADS2 knockdown on CRC cell behavior and ferroptosis markers.
  • Chemosensitivity assays to evaluate FADS2 knockdown effects on oxaliplatin treatment.

Main Results:

  • High FADS2 expression correlated with poorer CRC prognosis and increased immune cell infiltration.
  • FADS2 knockdown significantly promoted ferroptosis by altering glutathione (GSH), malondialdehyde (MDA), SLC7A11, and GPX4 levels.
  • Reduced FADS2 expression suppressed CRC cell proliferation, migration, and invasion, with partial rescue by SLC7A11 or GPX4 overexpression.
  • FADS2 knockdown enhanced CRC cell chemosensitivity to oxaliplatin.

Conclusions:

  • FADS2 is a key driver of CRC proliferation and tumor growth by inhibiting ferroptosis.
  • Targeting FADS2 presents a promising therapeutic strategy to induce ferroptosis and suppress CRC progression.
  • FADS2 inhibition enhances oxaliplatin efficacy in CRC, offering potential for improved clinical outcomes.