Involvement of ROS and JNK1 in selenite-induced a poptosisin Chang liver cells

Kim, Yong-Sook; Jhon, Deok-Young; Lee, Kee‐Young

doi:10.1038/emm.2004.22

Cited by 68 publications

(38 citation statements)

References 31 publications

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“…In this study, we investigated proton beam with single treatment induced tumor cell death cultivated as a monolayer in vitro condition and a possible mechanism by which proton beam induces tumor cell apoptosis. ROS promote apoptosis by stimulating pro-apoptotic signaling molecules such as ASK1, JNK and p38 MAPK (Benhar et al, 2001;Jr Davis et al, 2001;Tobiume et al, 2001;Kim et al, 2004). Activation of JNK and p38 MAPK in proton likely mediates apoptosis induced by proton.…”

Section: Discussionmentioning

confidence: 99%

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Lee

Park

et al. 2008

Exp Mol Med

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Proton beam is useful to target tumor tissue sparing normal cells by allowing precise dose only into tumor cells. However, the cellular and molecular mechanisms by which proton beam induces tumor cell death are still undefined. We irradiated three different tumor cells (LLC, HepG2, and Molt-4) with low energy proton beam (35 MeV) with spread out Bragg peak (SOBP) in vitro, and investigated cell death by MTT or CCK-8 assay at 24 h after irradiation. LLC and HepG2 cells were sensitive to proton beam at over 10 Gy to induce apoptosis whereas Molt-4 showed rather low sensitivity. Relative biological effectiveness (RBE) values for the death rate relative to γ-ray were ranged from 1.1 to 2.3 in LLC and HepG2 but from 0.3 to 0.7 in Molt-4 at 11 d after irradiation by colony formation assay. The typical apoptotic nuclear DNA morphological pattern was observed by staining with 4'-6-diamidino-2-phenylindole (DAPI). Tiny fragmented DNA was observed in HepG2 but not in Molt-4 by the treatment of proton in apoptotic DNA fragment assay. By FACS analysis after stained with FITC-Annexin-V, early as well as median apoptotic fractions were clearly increased by proton treatment. Proton beam-irradiated tumor cells induced a cleavage of poly (ADP-ribose) polymerase-1 (PARP-1) and procaspases-3 and -9. Activity of caspases was highly enhanced after proton beam irradiation. Reactive oxygen species (ROS) were significantly increased and N-acetyl cysteine pretreatment restored the apoptotic cell death induced by proton beam. Furthermore, p38 and JNK but not ERK were activated by proton and dominant negative mutants of p38 and JNK revived proton-induced apoptosis, suggesting that p38 and JNK pathways may be activated through ROS to activate apoptosis. In conclusion, our data clearly showed that single treatment of low energy proton beam with SOBP increased ROS and induced cell death of solid tumor cells (LLC and HepG2) in an apoptotic cell death program by the induction of caspases activities.

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Section: Discussionmentioning

confidence: 99%

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Lee

Park

et al. 2008

Exp Mol Med

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“…The finding that pharmacologic and genetic interruption of the JNK pathway attenuated 2ME-mediated lethality indicates that stress pathways play a critical functional role in apoptosis induction by this agent. The mechanism by which oxidative stress triggers JNK activation is not known with certainty, but may involve release from GSH-mediated inhibitory effects (Kim et al, 2004) or, alternatively, perturbations in thioredoxin, leading to activation of ASK-1 (apoptosis signal-regulating kinase-1), of which JNK is a downstream target . Interestingly, ectopic expression of Akt not only blocked 2ME-mediated mitochondrial injury and apoptosis but also prevented the striking increase in JNK activation, raising the possibility that one of the mechanisms by which Akt protects cells from 2ME lethality is by opposing JNK activation.…”

Section: Figurementioning

confidence: 99%

2-Methoxyestradiol-induced apoptosis in human leukemia cells proceeds through a reactive oxygen species and Akt-dependent process

et al. 2005

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“…The c-Jun/AP-1 transcriptional factor has been of great interest to researchers because its activity is influenced by oxidative stress and can induce apoptosis (Sawai et al, 1995;Gong et al, 2004;Kim et al, 2004). TAJ, also known as TROY, is a -46 kDa membrane protein possessing characteristic cysteine-rich motifs in the extracellular domain and a TNF receptor-associated factor (TRAF)-2 binding sequence in the cytoplasmic domain (Eby et al, 2000).…”

Section: Activation Of Stress-associated Proteinsmentioning

confidence: 99%

Activation of the intrinsic mitochondrial apoptotic pathway in swine influenza virus-mediated cell death

Choi

Kim²,

Kim³

et al. 2006

Exp Mol Med

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Involvement of ROS and JNK1 in selenite-induced a poptosisin Chang liver cells

Cited by 68 publications

References 31 publications

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

2-Methoxyestradiol-induced apoptosis in human leukemia cells proceeds through a reactive oxygen species and Akt-dependent process

Activation of the intrinsic mitochondrial apoptotic pathway in swine influenza virus-mediated cell death

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