Studies on promotion of hematopoietic tumor cell survival by A20

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A20 is a ubiquitin-editing enzyme that regulates inflammation and cancer development. Our current studies revealed that A20 was abundantly expressed in several types of cancer cells such as HTLV-I infected cells in contrast to lymphomas of B-cell lineage that harbor somatic mutation or deletion. In HTLV-I infected cell lines, A20 was co-immunoprecipitated with caspase-8 or FADD independently of any death-ligand stimulation. RNA-interference mediated depletion of A20 induced activation of caspase-8 and its downstream effectors, caspase-3 and -7, and caused marked reduction in the cell viability. Taken together, these results suggest that A20 plays a pivotal role in the survival of HTLV-I-infected cells.