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Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma

Bradley D Shields1, Brian Koss1, Erin M Taylor1

  • 1Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas.

Cancer Research
|January 25, 2019
PubMed

Insights

E-cadherin expression in melanoma tumors enhances immune attack and improves response to immune checkpoint blockade (ICB) therapy. This finding offers a new strategy to overcome resistance in cancer treatment.

Area of Science:

  • Oncology
  • Immunology
  • Cancer Research

Background:

  • Checkpoint blockade therapies are crucial in oncology.
  • Malignant melanoma resistant to these therapies often shows mesenchymal transition and E-cadherin loss.
  • Understanding resistance mechanisms is vital for improving cancer treatment.

Purpose of the Study:

  • To investigate the role of E-cadherin in mediating anti-tumor immune response and responsiveness to immune checkpoint blockade (ICB) in melanoma.
  • To provide in vivo evidence for E-cadherin's function in facilitating immune attack.

Main Methods:

  • Exogenously expressed E-cadherin in a B16F10 melanoma mouse model (B16.Ecad).
  • Assessed tumor growth, metastatic potential, and survival in vivo.
  • Transplanted B16.Ecad into immunodeficient (Rag1-/-) and CD103-deficient mice.
  • Evaluated responsiveness to combination immune checkpoint blockade (ICB).

Main Results:

  • B16.Ecad tumors exhibited delayed growth, reduced metastasis, and increased survival compared to controls.
  • Tumor growth delay was abrogated in Rag1-/- and CD103-/- mice, indicating immune and CD103+ cell mediation.
  • B16.Ecad tumors showed enhanced responsiveness to combination ICB therapy.

Conclusions:

  • E-cadherin expression on tumor cells facilitates immune attack against melanoma.
  • E-cadherin is a key factor in overcoming resistance to immune checkpoint blockade.
  • Amplifying CD103+ immune cell subsets presents a potential therapeutic strategy for E-cadherin-expressing malignancies.

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