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Calcium depletion enhances nectin-1 expression and herpes oncolytic therapy of squamous cell carcinoma

Z Yu1, S Li, Y-Y Huang

  • 1Head and Neck Service, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.

Cancer Gene Therapy
|May 26, 2007
PubMed

Insights

Calcium depletion enhances oncolytic herpes simplex virus type 1 (HSV-1) therapy for squamous cell carcinoma (SCC) by increasing nectin-1 receptor expression. This strategy improves viral entry and tumor regression, offering a novel approach to cancer treatment.

Area of Science:

  • Oncology
  • Virology
  • Biotechnology

Background:

  • Attenuated, oncolytic herpes simplex virus type 1 (HSV-1) show promise in preclinical cancer models.
  • Nectin-1, a receptor for HSV-1 glycoprotein D, is also part of intercellular adherens junctions (AJs).

Purpose of the Study:

  • To investigate if disrupting AJs via calcium depletion can increase nectin-1 exposure and enhance HSV-1 oncolytic therapy in squamous cell carcinoma (SCC).

Main Methods:

  • Utilized calcium depletion in SCC cell lines and murine SCC flank tumors.
  • Administered NV1023, an oncolytic HSV-1, with and without ethylenediaminetetraacetic acid (EDTA).
  • Assessed nectin-1 expression, viral entry, binding, cytotoxicity, and tumor regression.

Main Results:

  • Calcium depletion increased nectin-1 expression and cell separation in SCC cell lines.
  • NV1023 viral entry, soluble gD protein binding, and cytotoxicity were enhanced under low calcium conditions.
  • Combined NV1023 and EDTA treatment significantly improved tumor regression in murine SCC models.

Conclusions:

  • Disrupting adherens junctions by calcium depletion enhances nectin-1 receptor expression on cancer cells.
  • This modulation strategy significantly improves the efficacy of oncolytic HSV-1 therapy.
  • This approach holds potential for enhancing therapies using various herpes vectors.

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