2015
DOI: 10.1038/cddis.2015.276
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Caspase-3 feedback loop enhances Bid-induced AIF/endoG and Bak activation in Bax and p53-independent manner

Abstract: Chemoresistance in cancer has previously been attributed to gene mutations or deficiencies. Bax or p53 deficiency can lead to resistance to cancer drugs. We aimed to find an agent to overcome chemoresistance induced by Bax or p53 deficiency. Here, we used immunoblot, flow-cytometry analysis, gene interference, etc. to show that genistein, a major component of isoflavone that is known to have anti-tumor activities in a variety of models, induces Bax/p53-independent cell death in HCT116 Bax knockout (KO), HCT116… Show more

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Cited by 37 publications
(34 citation statements)
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“…EndoG translocation was originally reported to occur in a caspase-independent manner [27] , whereas the release of this nuclease from mitochondria was described to require caspase activation [45] . Positive feedback loop of caspase-3 was proposed to be mediated by the release of AIF/EndoG [46] . However, EndoG is not likely to be involved in daunorubicin-induced apoptosis of miPS-LLCcm cells, given that EndoG translocation from mitochondria to nuclei was not detected in the preliminary experiment [ Supplementary Figure 2].…”
Section: Discussionmentioning
confidence: 99%
“…EndoG translocation was originally reported to occur in a caspase-independent manner [27] , whereas the release of this nuclease from mitochondria was described to require caspase activation [45] . Positive feedback loop of caspase-3 was proposed to be mediated by the release of AIF/EndoG [46] . However, EndoG is not likely to be involved in daunorubicin-induced apoptosis of miPS-LLCcm cells, given that EndoG translocation from mitochondria to nuclei was not detected in the preliminary experiment [ Supplementary Figure 2].…”
Section: Discussionmentioning
confidence: 99%
“…Meanwhile, BetA also induced casapse-3 cleavage and changes in Akt phosphorylation in 8226 cells ( Supplementary Figure 5A ). Considering that Akt is an upstream anti-apoptotic regulatory molecule [ 9 , 56 58 ], we speculated that inactivation of Akt is required for BetA-induced apoptosis.…”
Section: Resultsmentioning
confidence: 99%
“…Apoptosis may result in abnormal expression of Bcl-2 family members including Bcl-2 and Bax, which are key regulators of cell apoptosis and play pivotal roles in anti-apoptotic and pro-apoptotic, respectively [17]. Furthermore, p53 is a very important tumor suppressor protein that mediates the stressinduced apoptosis cascade [18,19].…”
Section: Discussionmentioning
confidence: 99%