Title : ROS Accumulation by PEITC Selectively Kills Ovarian Cancer Cells via UPR-Mediated Apoptosis.

Pub. Date : 2015

PMID : 26284193






4 Functional Relationships(s)
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1 The key regulator of UPR-mediated apoptosis, CHOP/GADD153 and endoplasmic reticulum resident chaperone BiP/GRP78 were parallely up-regulated with activation of two major sensors of the UPR [PERK and ATF-6 in PA-1; PERK, and IRE1alpha in SKOV-3) in response to ROS accumulation induced by PEITC (5 muM). Reactive Oxygen Species DNA damage inducible transcript 3 Homo sapiens
2 The key regulator of UPR-mediated apoptosis, CHOP/GADD153 and endoplasmic reticulum resident chaperone BiP/GRP78 were parallely up-regulated with activation of two major sensors of the UPR [PERK and ATF-6 in PA-1; PERK, and IRE1alpha in SKOV-3) in response to ROS accumulation induced by PEITC (5 muM). Reactive Oxygen Species DNA damage inducible transcript 3 Homo sapiens
3 ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the effect of PEITC on UPR signatures (P-PERK, IRE1alpha, CHOP/GADD153, and BiP/GRP78), suggesting the involvement of ROS in UPR-mediated apoptosis. Reactive Oxygen Species DNA damage inducible transcript 3 Homo sapiens
4 ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the effect of PEITC on UPR signatures (P-PERK, IRE1alpha, CHOP/GADD153, and BiP/GRP78), suggesting the involvement of ROS in UPR-mediated apoptosis. Reactive Oxygen Species DNA damage inducible transcript 3 Homo sapiens