RT Journal Article SR Electronic T1 Mutant KRAS Promotes NKG2D+ T Cell Infiltration and CD155 Dependent Immune Evasion JF Anticancer Research JO Anticancer Res FD International Institute of Anticancer Research SP 4663 OP 4674 DO 10.21873/anticanres.14465 VO 40 IS 8 A1 KENSUKE NISHI A1 SHUHEI ISHIKURA A1 MASAYO UMEBAYASHI A1 TAKASHI MORISAKI A1 TAKASHI INOZUME A1 TETSUSHI KINUGASA A1 MIKIKO AOKI A1 SATOSHI NIMURA A1 ANTHONY SWAIN A1 YOICHIRO YOSHIDA A1 SUGURU HASEGAWA A1 KAZUKI NABESHIMA A1 TOSHIFUMI SAKATA A1 SENJI SHIRASAWA A1 TOSHIYUKI TSUNODA YR 2020 UL http://ar.iiarjournals.org/content/40/8/4663.abstract AB Background/Aim: Roles for mutant (mt) KRAS in the innate immune microenvironment in colorectal cancer (CRC) were explored. Materials and Methods: Human CRC HCT116-derived, mtKRAS-disrupted (HKe3) cells that express exogenous mtKRAS and allogenic cytokine-activated killer (CAK) cells were co-cultured in 3D floating (3DF) culture. The anti-CD155 antibody was used for function blocking and immuno histochemistry. Results: Infiltration of CAK cells, including NKG2D+ T cells, into the deep layer of HKe3-mtKRAS spheroids, was observed. Surface expression of CD155 was found to be up-regulated by mtKRAS in 3DF culture and CRC tissues. Further, the number of CD3+ tumor-infiltrating cells in the invasion front that show substantial CD155 expression was significantly larger than the number showing weak expression in CRC tissues with mtKRAS. CD155 blockade decreased the growth of spheroids directly and indirectly through the release of CAK cells. Conclusion: CD155 blockade may be useful for therapies targeting tumors containing mtKRAS.