Abstract
Background TRAIL, a member of the TNF ligand family, was shown to selectively kill cancer cells and, therefore, to participate in the cell-mediated immunity against tumors. However, TRAIL is down-regulated in a variety of cancers. Furthermore, PRAME (preferentially expressed antigen of melanoma) is frequently over expressed in a wide variety of malignant diseases. It was shown that PRAME, in a complex with a member of the polycomb group, EZH2, can function as a transcriptional repressor of retinoic acid receptor. Interestingly, TRAIL expression can be positively regulated by retinoic acid. Previous studies performed by us revealed that TRAIL is down-regulated and PRAME is up-regulated during development of chronic myeloid leukemia (CML) and that their normal levels are restored after complete cytogenetic remission (CCR). There was a significant, negative correlation between the expression of PRAME and TRAIL in CML patients. Over expression of BCR-ABL in the acute promyelocytic leukemia cell line HL-60 increased the levels of PRAME and decreased the levels of TRAIL. Knocking-down of either PRAME or EZH2 in K562 CML cell line resulted in TRAIL up-regulation.
Highlights
TRAIL, a member of the TNF ligand family, was shown to selectively kill cancer cells and, to participate in the cell-mediated immunity against tumors
It was shown that PRAME, in a complex with a member of the polycomb group, EZH2, can function as a transcriptional repressor of retinoic acid receptor
TRAIL expression can be positively regulated by retinoic acid
Summary
Background TRAIL, a member of the TNF ligand family, was shown to selectively kill cancer cells and, to participate in the cell-mediated immunity against tumors. TRAIL is down-regulated in a variety of cancers.
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