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Related Experiment Video

Updated: Jun 25, 2026

Screening Ion Channels in Cancer Cells

Screening Ion Channels in Cancer Cells

Published on: June 16, 2023

Mutant sodium channel for tumor therapy.

Bakhos A Tannous¹, Adam P Christensen, Lisa Pike

¹Department of Neurology, Molecular Neurogenetics Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02129, USA. btannous@hms.harvard.edu

Molecular Therapy : the Journal of the American Society of Gene Therapy

|March 5, 2009

Summary

This study introduces a novel cancer therapy using a modified sodium channel delivered by a viral vector. This approach rapidly kills tumor cells and adjacent connected cells, offering a new treatment strategy.

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Mutagenesis and Functional Analysis of Ion Channels Heterologously Expressed in Mammalian Cells

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Last Updated: Jun 25, 2026

Screening Ion Channels in Cancer Cells

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Published on: June 16, 2023

Radionuclide-fluorescence Reporter Gene Imaging to Track Tumor Progression in Rodent Tumor Models

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Mutagenesis and Functional Analysis of Ion Channels Heterologously Expressed in Mammalian Cells

Mutagenesis and Functional Analysis of Ion Channels Heterologously Expressed in Mammalian Cells

Published on: October 1, 2010

Area of Science:

Oncology
Molecular Biology
Virology

Background:

Viral vectors are utilized for delivering therapeutic genes to tumors.
Developing novel gene therapies for cancer remains a critical research area.

Purpose of the Study:

To investigate a novel tumor therapy using a constitutively open mammalian brain sodium channel, ASIC2a.
To evaluate the efficacy of delivering this mutant channel via a herpes simplex virus-1/Epstein-Barr virus (HSV/EBV) hybrid amplicon vector.

Main Methods:

Gene delivery using a HSV/EBV hybrid amplicon vector with a tetracycline-inducible system (tet-on).
Assessment of sodium influx using patch clamp recording and sodium imaging in cultured tumor cells.
Evaluation of tumor regression in nude mice via intratumoral injection and systemic doxycycline administration, monitored by in vivo bioluminescence imaging.

Main Results:

Delivery of the mutant ASIC2a channel led to amiloride-sensitive sodium influx and rapid tumor cell death (swelling and lysis) within hours.
Adjacent, non-infected tumor cells connected by gap junctions also succumbed to the therapy.
Significant regression of subcutaneous tumors was observed in mice treated with the vector and doxycycline.

Conclusions:

The engineered viral vector effectively delivers and expresses the mutant sodium channel, inducing rapid tumor cell death.
This oncolytic strategy impacts both infected and connected non-infected tumor cells, suggesting a bystander effect.
The therapy demonstrates potential for rapid and effective tumor eradication, overcoming resistance mechanisms.