Abstract:
:Various molecular mechanisms are involved in the efficacy of arsenic trioxide (ATO) against malignant hematologic and some solid tumors. FLICE-like inhibitory protein (FLIP) is an inhibitor of apoptosis mediated by death receptors. In this study, we identified a new link between the down-regulation of cellular FLIP(L) and ATO-induced autophagy. ATO induced the degradation of FLIP(L) in K562 and MGC803 cells, which was mediated by the ubiquitin-proteasome pathway. Moreover, the casitas B-lineage lymphoma-b (Cbl-b) was involved in this process, which interacted with FLIP(L) and promoted proteasomal degradation of FLIP(L). Our findings lead to a better understanding of the mechanism of action of ATO, and suggest that a novel signaling pathway is required for ATO-induced autophagy in K562 and MGC803 cells.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Zhang G,Liu J,Zhang Y,Qu J,Xu L,Zheng H,Liu Y,Qu Xdoi
10.1016/j.febslet.2012.07.067subject
Has Abstractpub_date
2012-09-21 00:00:00pages
3104-10issue
19eissn
0014-5793issn
1873-3468pii
S0014-5793(12)00635-7journal_volume
586pub_type
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