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 Videos

Elucidation of stannin function using microarray analysis: implications for cell cycle control.

Brian E Reese1, Dan Krissinger, Jong K Yun

  • 1Department of Pharmacology, Penn State College of Medicine, Hershey, PA 17033, USA.

Gene Expression
|April 1, 2006
PubMed
Summary

Stannin (Snn) protein regulates tumor necrosis factor-alpha (TNF-alpha)-induced growth arrest in human umbilical vein endothelial cells (HUVECs). Snn knockdown significantly inhibits HUVEC growth, suggesting its role in TNF-alpha signaling pathways.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Cannabinoid-Induced Immunogenic Cell Death of Colorectal Cancer Cells Through De Novo Synthesis of Ceramide Is Partially Mediated by CB2 Receptor.

Cancers·2024
Same author

Fanning the Flames of Endoplasmic Reticulum (ER) Stress: Can Sphingolipid Metabolism Be Targeted to Enhance ER Stress-Associated Immunogenic Cell Death in Cancer?

Molecular pharmacology·2024
Same author

Characterization of Anticancer Effects of the Analogs of DJ4, a Novel Selective Inhibitor of ROCK and MRCK Kinases.

Pharmaceuticals (Basel, Switzerland)·2023
Same author

Regulatory Role of Sphingosine-1-Phosphate and C16:0 Ceramide, in Immunogenic Cell Death of Colon Cancer Cells Induced by Bak/Bax-Activation.

Cancers·2022
Same author

Inhibition of Sphingosine Kinase Activity Enhances Immunogenic Cell Surface Exposure of Calreticulin Induced by the Synthetic Cannabinoid 5-epi-CP-55,940.

Cannabis and cannabinoid research·2021
Same author

Sphingosine Kinase Inhibition Enhances Dimerization of Calreticulin at the Cell Surface in Mitoxantrone-Induced Immunogenic Cell Death.

The Journal of pharmacology and experimental therapeutics·2021

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Signal Transduction

Background:

  • Stannin (Snn) is a conserved vertebrate protein with an unclear cellular function.
  • Tumor necrosis factor-alpha (TNF-alpha) induces Snn gene expression in human umbilical vein endothelial cells (HUVECs) via protein kinase C-epsilon (PKC-epsilon).
  • TNF-alpha stimulation in HUVECs leads to altered gene expression and cell growth inhibition.

Purpose of the Study:

  • To investigate the role of Stannin (Snn) in TNF-alpha-induced signaling and HUVEC growth arrest.
  • To identify genes regulated by Snn in response to TNF-alpha stimulation.
  • To elucidate the mechanism by which Snn influences the cell cycle.

Main Methods:

  • Gene expression analysis using microarray in TNF-alpha-stimulated HUVECs with and without Snn knockdown via siRNA.

Related Experiment Videos

  • Quantitative analysis of differentially expressed genes.
  • Cell cycle analysis using flow cytometry.

    • Main Results:

    • Snn knockdown significantly inhibited HUVEC growth following TNF-alpha treatment.
    • Microarray analysis revealed 96 differentially expressed genes between TNF-alpha-stimulated HUVECs and those with Snn knockdown.
    • Upregulation of cell cycle regulators, including interleukin-4, p29, WT1/PRKC, HRas-like suppressor, and MDM4, was observed.
    • Flow cytometry confirmed a significant increase in G1 cell cycle arrest in HUVECs with Snn knockdown.

    Conclusions:

    • Stannin (Snn) plays a functional role in regulating TNF-alpha-induced signaling pathways.
    • Snn is involved in the control of HUVEC growth arrest and cell cycle progression.
    • These findings suggest Snn as a key mediator in the cellular response to TNF-alpha.