2014
DOI: 10.1016/j.cbi.2014.03.010
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Cordycepin induces apoptosis of C6 glioma cells through the adenosine 2A receptor-p53-caspase-7-PARP pathway

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Cited by 59 publications
(44 citation statements)
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“…Lee and co-workers [20] suggested that cordycepin could inhibit the migration and invasion of LNCap human prostate carcinoma cells by inactivation of AKT, resulting in the down-regulation of the TJs (Tight Junctions) and MMPs (Matix Metalloproteinases). Chen and co-workers [21] investigated the effect of cordycepin on C6 glioma cells and showed that cordycepin could induce the apoptosis of C6 glioma cells via the adenosine 2A receptor-p53-caspase-7-PARP pathway. Though almost all the studies reported that cordycepin could inhibit cell proliferation and induce apoptosis, the concrete mechanisms were not identical.…”
Section: Introductionmentioning
confidence: 99%
“…Lee and co-workers [20] suggested that cordycepin could inhibit the migration and invasion of LNCap human prostate carcinoma cells by inactivation of AKT, resulting in the down-regulation of the TJs (Tight Junctions) and MMPs (Matix Metalloproteinases). Chen and co-workers [21] investigated the effect of cordycepin on C6 glioma cells and showed that cordycepin could induce the apoptosis of C6 glioma cells via the adenosine 2A receptor-p53-caspase-7-PARP pathway. Though almost all the studies reported that cordycepin could inhibit cell proliferation and induce apoptosis, the concrete mechanisms were not identical.…”
Section: Introductionmentioning
confidence: 99%
“…PARP plays a pivotal role particularly in the maintenance of genomic DNA stability, apoptosis and in the response to oxidative stress (Decker and Muller, 2002). Although the role of PARP and caspase-3 in cellular apoptotic signaling pathway have been recognized for some time and gradually known to contribute to lethal effect of chemo-radiotherapy, the exact upstream triggering events leading to activation of this pathway remain unclear (Siegel and McCullough, 2011;Chen et al, 2014). Bcl-2 family members are regulated on the transcriptional level: several pro-survival genes (such as Bcl-2 and Bcl-XL) are induced transcriptionally by certain cytokines, and Bax expression is controlled by several transcription factors including the tumor suppressor proteins P53 and P73 (Adams and Cory, 1998;Muscolini et al, 2008;De et al, 2014).…”
Section: Resultsmentioning
confidence: 99%
“…The cytochrome c along with apoptotic protease activating factor-1 (Apaf-1), procaspase-9 and ATP could form multiprotein complex (apotosome) in cytoplasm (Zhang, 2007). Then the caspase recruitment domain (CARD) of procaspase-9 and Apaf-1 was activated, and effective caspases, such as caspase-3, caspase-6, and caspase-7, were thus activated (Chen et al, 2014;Licht et al, 2014). Finally, cancer cells apoptosis took place.…”
Section: Discussionmentioning
confidence: 99%