2012
DOI: 10.1038/onc.2012.7
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New frontiers in promoting tumour cell death: targeting apoptosis, necroptosis and autophagy

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Cited by 188 publications
(159 citation statements)
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References 176 publications
(210 reference statements)
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“…Here, we found that the promoter region of miR-200c was hypermethylated in renal carcinoma cell lines treated with sorafenib or imatinib than control, suggesting epigenetic mechanisms might be also involved in ccRCC treatment-resistant. We Heme oxygenase-1 (HO1), an anti-apoptotic gene, was involved in imatinib resistance in cancers [19] and the regulation of autophagy [20]. Mechanically, HO-1 transcriptionally involved in Beclin-1 and Bcl-2 signaling pathway, which has been reported essential for tumor growth and autophagy [21].…”
Section: Discussionmentioning
confidence: 99%
“…Here, we found that the promoter region of miR-200c was hypermethylated in renal carcinoma cell lines treated with sorafenib or imatinib than control, suggesting epigenetic mechanisms might be also involved in ccRCC treatment-resistant. We Heme oxygenase-1 (HO1), an anti-apoptotic gene, was involved in imatinib resistance in cancers [19] and the regulation of autophagy [20]. Mechanically, HO-1 transcriptionally involved in Beclin-1 and Bcl-2 signaling pathway, which has been reported essential for tumor growth and autophagy [21].…”
Section: Discussionmentioning
confidence: 99%
“…Subsequently, AIF translocates to the nucleus and provokes chromatin condensation and DNA fragmentation [77]. Necroptosis or regulated necrosis also involves PARP activation [78]. Therefore, PARP can participate in different types of cell death and it is not exclusive of apoptosis, as previously thought.…”
Section: Parp Proteolysis As An Indicator Of Cell Deathmentioning
confidence: 81%
“…A novel death regulation platform named ripoptosome has recently been described. Unlike complex II, the ripoptosome forms independently of death receptors, is activated by genotoxic stress or IAP antagonists and is tightly regulated by IAPs (ciAP1, cIAP2, xIAP) or cellular FLICE-like inhibitory protein (FLIP), a catalytically inactive homologue of caspase-8 [78,90,91]. The executioner mechanisms of necroptosis are unclear.…”
Section: Necroptosismentioning
confidence: 99%
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“…Cancer is a multifactoral disease, with a consequence of the unusual mechanisms of genetic, metabolic or biochemical factors, which basically spoil the controlled proliferation and/or apoptosis mechanism of the cells [1]. The unlimited ability of proliferation, the developed resistance against apoptotic signals, the capability of invasion, metastasis and angiogenesis, abnormal activity of energy metabolism and the defence against immune attack are the hallmarks of cancer [2,3].…”
Section: Introductionmentioning
confidence: 99%