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- W2416789747 abstract "2468 The RNase III endonuclease Dicer plays a key role in generation of mature, approximately 22-nucleotide-long micro RNAs (miRNAs) in cells. Recent studies suggest that Dicer is required for Type-2 T-cell response, which counteracts anti-tumor immunity. Furthermore, Dicer expression is associated with malignant phenotype of prostate cancers through regulation of miRNAs. These observations led us to hypothesize that expression of Dicer in cancer cells might regulate their susceptibility against immune-surveillance through processing of miRNAs. Among three human colorectal cancer cell lines (HCT116, DLD-1 and RKO) in which exon 5 of the human Dicer gene is disrupted (ex5-/-) (Cummins, J.M et al. 2006), HCT116 (ex5-/-) cells expressed human leukocyte antigen (HLA)-A2 as well as tumor antigens interleukin-13 receptor alpha2 (IL-13Rα2) and EphA2. Compared to wild-type HCT116 cells, HCT116 (ex5-/-) cells were found to be remarkably more susceptible to antigen-specific lysis by cytotoxic T lymphocytes (CTLs) raised against IL-13Rα2 or EphA2. To identify causative molecules that promoted the susceptibility of HCT116 (ex5-/-) cells, we examined expression of a panel of proteins that are known to mediate CTL-tumor cell interactions, including HLA class I, intercellular cell adhesion molecule (ICAM)-1, Fas, CD40, death receptor (DR)5 as well as tumor antigens IL-13Rα2 and EphA2 in the three ex5-/- cell lines and corresponding wild-type cells. Among these, ICAM-1 was up-regulated in all ex5-/- cell lines, while none of the other molecules evaluated were differentially expressed in ex5-/- vs. wild-type cells. Antibody-mediated blockade of the ICAM-1-LFA-1 interaction inhibited the specific lysis of the CTLs against HCT116 (ex5-/-) cells, indicating a pivotal role of this interaction. We next sought to identify specific miRNAs that can modulate ICAM-1 expression. Based on the miRBase algorithm (http://microrna.sanger.ac.uk), miRNAs 222 and 339 were predicted to bind to ICAM-1. Indeed, quantitative RT-PCR analysis showed the decrease of miRNAs 222 and 339 in all three ex5-/- cell lines compared to wild-type lines. Moreover, inhibition of these miRNAs in the parental cells by transfection with anti-miRNA 222 and 339 RNA-based inhibitor constructs up-regulated ICAM-1 expression and susceptibility of these cells against CTLs. Taken together, our results suggest that Dicer is responsible for the generation of miR-222 and miR-339, which suppress ICAM-1 expression on cancer cells, thereby down-regulating the susceptibility of cancer cells to CTL-mediated lysis." @default.
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- W2416789747 date "2008-05-01" @default.
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- W2416789747 title "Dicer-regulated micro RNAs 222 and 339 promote immune-escape of cancer cells through downregulation of ICAM-1" @default.
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