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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Oncotarget 2015 ; 6 (4): 1995-2008 Nephropedia Template TP
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Neoalbaconol induces cell death through necroptosis by regulating RIPK-dependent autocrine TNF? and ROS production #MMPMID25575821
Yu X; Deng Q; Li W; Xiao L; Luo X; Liu X; Yang L; Peng S; Ding Z; Feng T; Zhou J; Fan J; Bode AM; Dong Z; Liu J; Cao Y
Oncotarget 2015[Feb]; 6 (4): 1995-2008 PMID25575821show ga
Necroptosis/regulated necrosis is a caspase-independent, but receptor interacting protein kinase (RIPK)-dependent form of cell death. In previous studies, neoalbaconol (NA), a constituent extracted from Albatrellus confluens, was demonstrated to induce necroptosis in some cancer cell lines. The molecular mechanism of NA-induced necroptosis is described in this research study. We determined that NA-induced cell death is partly dependent on tumor necrosis factor ? (TNF?) feed-forward signaling. More importantly, NA abolished the ubiquitination of RIPK1 by down-regulating E3 ubiquitin ligases, cellular inhibitors of apoptosis protein 1/2 (cIAP1/2) and TNF? receptor-associated factors (TRAFs). The suppression of RIPK1 ubiquitination induced the activation of the non-canonical nuclear factor-?B (NF-?B) pathway and stimulated the transcription of TNF?. Moreover, we also found that NA caused RIPK3-mediated reactive oxygen species (ROS) production and contribution to cell death. Taken together, these results suggested that two distinct mechanisms are involved in NA-induced necroptosis and include RIPK1/NF-?B-dependent expression of TNF? and RIPK3-dependent generation of ROS.