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Mutant KRAS Promotes NKG2D+ T Cell Infiltration and CD155 Dependent Immune Evasion

Kensuke Nishi1,2,3, Shuhei Ishikura1,4, Masayo Umebayashi5

  • 1Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.

Anticancer Research
|July 31, 2020
PubMed
Abstract

Insights

Mutant KRAS in colorectal cancer (CRC) upregulates CD155, attracting immune cells. Blocking CD155 may offer a new therapy for CRC tumors with mutant KRAS.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Mutant KRAS (mtKRAS) plays a role in colorectal cancer (CRC) development.
  • The innate immune microenvironment's interaction with mtKRAS in CRC is not fully understood.

Purpose of the Study:

  • To investigate the role of mtKRAS in the innate immune microenvironment of CRC.
  • To explore the potential of targeting CD155 for CRC therapy.

Main Methods:

  • Co-culture of mtKRAS-expressing CRC cells (HKe3) with cytokine-activated killer (CAK) cells in 3D floating (3DF) culture.
  • Utilized anti-CD155 antibody for function blocking and immunohistochemistry.

Main Results:

  • Observed infiltration of CAK cells, including NKG2D+ T cells, into mtKRAS-expressing CRC spheroids.
  • mtKRAS upregulates surface CD155 expression in 3DF culture and CRC tissues.
  • CD155 blockade reduced spheroid growth directly and via CAK cell release, correlating with CD3+ cell infiltration in CRC tissues.

Conclusions:

  • CD155 upregulation by mtKRAS influences immune cell infiltration in CRC.
  • CD155 blockade demonstrates therapeutic potential for mtKRAS-driven CRC.
Keywords:
3D cultureCAK cellsCD155KRASPD-1TIGITTNK cells

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