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

Human tumor cells resistant to verapamil.

K R Huber1, W F Schmidt, B al-Assaad

  • 1Children's Cancer Research Laboratory, Department of Pediatrics, School of Medicine, University of South Carolina, Columbia 29208.

Biochemical and Biophysical Research Communications
|June 30, 1989
PubMed
Summary

Verapamil resistance in medulloblastoma cells stems from a stable phenotypic alteration, not P-glycoprotein. This resistance impacts cell proliferation and persists even after drug removal.

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

Gene expression profiles induced by growth factors in in vitro cultured osteoblasts.

Bone & joint research·2014
Same author

Quantitative structure-activity relationships (QSAR) of trimedlure isomers.

Journal of chemical ecology·2013
Same author

Structure-activity relationship observations oftrans-trimedlure enantiomers.

Journal of chemical ecology·2013
Same author

The role of memory-related gene polymorphisms, KIBRA and CLSTN2, on replicate memory assessment in the elderly.

Journal of neural transmission (Vienna, Austria : 1996)·2011
Same author

Biodegradability of injection molded bioplastic pots containing polylactic acid and poultry feather fiber.

Bioresource technology·2011
Same author

Risk factors for cerebrovascular and cardiovascular diseases beyond age 75 years.

Journal of neural transmission (Vienna, Austria : 1996)·2010

Area of Science:

  • Pharmacology
  • Cancer Biology
  • Molecular Biology

Background:

  • Verapamil exhibits dual effects: enhancing chemotherapy at low doses and inhibiting cell proliferation at high doses.
  • The mechanisms behind verapamil's diverse effects, particularly its antiproliferative action, require further elucidation.
  • Human brain tumor cell lines were utilized to investigate verapamil's antiproliferative mechanism.

Purpose of the Study:

  • To investigate the mechanisms underlying verapamil's antiproliferative effect.
  • To develop and characterize verapamil-resistant human brain tumor cell lines.
  • To understand the nature of the stable phenotypic alteration conferring verapamil resistance.

Main Methods:

  • Selection of TE671 medulloblastoma and A172 glioma cell lines for resistance to 100 uM verapamil.

Related Experiment Videos

  • Assessment of cell growth rates in the presence and absence of verapamil.
  • Evaluation of cell cycle phase alterations and c-myc gene expression.
  • Testing for cross-resistance to vincristine and adriamycin.
  • Analysis of P-glycoprotein expression.

    • Main Results:

    • Selected TE671 cells demonstrated stable resistance to verapamil's antiproliferative effects, maintaining growth similar to sensitive cells without verapamil.
    • Resistance persisted for at least three days post-verapamil removal, with minimal cell cycle alterations.
    • c-myc gene expression remained unchanged after verapamil removal, suggesting a stable phenotypic modification.
    • Resistant cells were not cross-resistant to vincristine or adriamycin.
    • No increased expression of P-glycoprotein (170-180 kDa) was observed in resistant cells.

    Conclusions:

    • A stable phenotypic alteration, not P-glycoprotein upregulation, is responsible for verapamil resistance in TE671 medulloblastoma cells.
    • The findings provide insights into the mechanisms of verapamil resistance and potential therapeutic strategies.
    • Further research is warranted to fully characterize the molecular basis of this stable resistance phenotype.