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 Experiment Video

Updated: Jul 1, 2026

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

Identification of Hub Genes, Single-Nucleotide Polymorphisms, and Potential Drug Targets In Breast Cancer Using

Xiaobo Jia1, Hui Su2, Jiaxin Zhang3

  • 1Department of Thyroid and Breast Surgery, The Affiliated Hospital of Xuzhou Medical University; x98013112@gmail.com.

Journal of Visualized Experiments : Jove
|June 29, 2026
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

Pharmacogenomics: Identification of New Drug Targets01:29

Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...

You might also read

Related Articles

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

Sort by
Same author

<i>Aeromonas salmonicida</i> isolated from pigs: Genomic and phenotypic antimicrobial resistance characterization.

Open veterinary journal·2026
Same author

Notch Signaling Regulates the Neuroprotective Effects of hUCMSCs in a Mouse Model of Cerebral Ischemia.

Journal of molecular neuroscience : MN·2026
Same author

Clinical characteristics and risk factors of protein-losing enteropathy: a retrospective study.

Frontiers in immunology·2026
Same author

Enhancing microbiologically influenced corrosion of Al-Zn-In-Cd sacrificial anode by Pseudomonas sp. in marine tidal environment.

Bioelectrochemistry (Amsterdam, Netherlands)·2026
Same author

Methodology and baseline characteristics of the China Migraine registry (CHIME): a nationwide, multi-center, prospective cohort study of 11,814 patients.

The journal of headache and pain·2026
Same author

Eu-proanthocyanidin/lactoferrin amyloid composite coating: interfacial microenvironment modulation for integrated enhancement of anti-inflammatory, antibacterial, and osteogenic effects.

Colloids and surfaces. B, Biointerfaces·2026
Same journal

A Video Protocol of a Randomized Controlled Clinical Trial - Electrochemotherapy of Cutaneous Metastases with Reduced Dose Bleomycin (BLESS Trial).

Journal of visualized experiments : JoVE·2026
Same journal

A Standardized Ex Vivo Porcine Oromucosal Model for Evaluating Peptide Fluxes.

Journal of visualized experiments : JoVE·2026
Same journal

Lightweight English Text Classification with Deep Learning Based on Complex System Theory.

Journal of visualized experiments : JoVE·2026
Same journal

Integrating Artificial Intelligence-Assisted Translation Support into English Courses: Effects on Translation Accuracy, Perceived Stress, and Anxiety.

Journal of visualized experiments : JoVE·2026
Same journal

A Toxin-Based Counter-Selection System for Markerless Gene Deletion and High-Density Tn5 Transposon Mutagenesis in Pectobacterium brasiliense.

Journal of visualized experiments : JoVE·2026
Same journal

Seamless Multimodal Human-Robot Communication: Integration Techniques in Human-Computer Interaction.

Journal of visualized experiments : JoVE·2026
See all related articles

MTHFD2 and PRDX3 genes are key regulators of mitochondrial oxidative stress in HER2-positive breast cancer, impacting drug resistance. Deleterious variants in these genes may alter redox balance and affect treatment outcomes.

Area of Science:

  • Biochemistry
  • Genetics
  • Oncology

Background:

  • HER2-positive breast cancer often develops resistance to therapies like Lapatinib.
  • Mitochondrial metabolic and redox reprogramming may play a role in this resistance.
  • Identifying biomarkers for resistance is crucial for improving treatment strategies.

Purpose of the Study:

  • To identify mitochondrial oxidative stress-related differentially expressed genes (MOS-DEGs) as potential biomarkers for therapeutic resistance in HER2-positive breast cancer.
  • To characterize the functional impacts of non-synonymous single nucleotide polymorphisms (nsSNPs) in these MOS-DEGs.
  • To investigate the structural and functional consequences of identified nsSNPs on protein activity.

Main Methods:

  • RNA-sequencing data analysis (GSE231524, GSE231525) using DESeq2 to identify DEGs.

Related Experiment Videos

Last Updated: Jul 1, 2026

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

  • Intersection of DEGs with mitochondrial oxidative stress genes to identify MOS-DEGs.
  • Functional enrichment, protein-protein interaction (PPI), Receiver Operating Characteristic (ROC) analysis, expression profiling, and survival analysis.
  • In silico evaluation of nsSNPs using multiple predictive tools and structural modeling (secondary and 3D) with molecular dynamics simulations.

    • Main Results:

    • MTHFD2 and PRDX3 were identified as central MOS-DEGs with opposing roles in mitochondrial redox metabolism.
    • MTHFD2 was significantly upregulated and associated with poor prognosis (HR = 1.53, p = 1.1 × 10⁻¹⁶), while PRDX3 showed protective expression (HR = 0.73, p = 7.7×10⁻¹⁰).
    • Five deleterious nsSNPs in MTHFD2 (e.g., rs1471336772) and four in PRDX3 (e.g., rs747786383) were identified, predicted to be damaging and potentially impair protein function and structural stability.

    Conclusions:

    • MTHFD2 and PRDX3 are key regulators of mitochondrial oxidative stress in HER2-positive breast cancer, influencing therapeutic resistance.
    • Deleterious nsSNPs in MTHFD2 and PRDX3 may contribute to altered redox balance, impacting metabolic adaptation and antioxidant defense.
    • These genes and their variants hold potential as biomarkers for predicting therapeutic response and understanding resistance mechanisms.