NF-κB protects rat ARL-6 hepatocellular carcinoma cells against hydrogen peroxide-induced apoptosis

Qiao, Liang; Yu, Jun; Dent, Paul; Farrell, Geoffrey C.

doi:10.4161/cbt.4.11.2078

Cited by 12 publications

(6 citation statements)

References 44 publications

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“…NF-κB p65 regulates telomerase activity by modulating the hTERT [29]. Functions of NF-κB in diverse tumor cells include maintaining proliferation and protecting cells from apoptosis [30]. Our data indicated that As 2 O 3 inhibited NF-κB activity in MUTZ-1 and SKM-1 cells, which is consistent with the finding that NF-κB inhibition contributes to arsenic-mediated induction of apoptosis as reported by Mathas et al [15].…”

Section: Discussionsupporting

confidence: 91%

Downregulation of hTERT: An Important As2O3 Induced Mechanism of Apoptosis in Myelodysplastic Syndrome

Wang

Tong

et al. 2014

PLoS ONE

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Two myelodysplastic syndrome (MDS) celllines, MUTZ-1 and SKM-1 cells, were used to study the effect of arsenic trioxide (As2O3) on hematological malignant cells. As2O3 induced this two cell lines apoptosis via activation of caspase-3/8 and cleavage of poly (ADP-ribose) polymerase (PARP), a DNA repair enzyme. As2O3 reduced NF-κB activity, which was important for inducing MUTZ-1 and SKM-1 cells apoptosis. As2O3 also inhibited the activities of hTERT in MUTZ-1 and SKM-1 cells. Moreover, the NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), had no effect on caspase-8 activation, although PDTC did inhibit MUTZ-1 and SKM-1 cells proliferation. Incubation of MUTZ-1 cells with a caspase-8 inhibitor failed to block As2O3-induced inhibition of NF-κB activity. Our findings suggest that As2O3 may induce apoptosis in MUTZ-1 and SKM-1 cells by two independent pathways: first, by activation of caspase-3/8 and PARP; and second, by inhibition of NF-κB activity, which results in downregulation of hTERT expression. We conclude that hTERT and NF-κB are important molecular targets in As2O3-induced apoptosis.

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Section: Discussionsupporting

confidence: 91%

Downregulation of hTERT: An Important As2O3 Induced Mechanism of Apoptosis in Myelodysplastic Syndrome

Wang

Tong

et al. 2014

PLoS ONE

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“…The concept that one therapeutic agent can activate pathways normally associated with cell survival has been well established over the past 15 years, and that inhibition of these survival pathway(s) causes a profound apoptotic response 5 - 8 . In APL cells inhibition of MEK1/2 was shown to enhance ATO toxicity and the findings in the present manuscript generally support the concept that this mechanism applies to other leukemic cell types 3 , 4 .…”

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confidence: 81%

Arsenic in leukemia

Dent¹

2013

Cancer Biology & Therapy

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It has been known for many years that arsenic trioxide (As2O3; ATO) is an effective therapy for acute promyelocytic leukemia but has little activity against other forms of the disease. ATO has diverse modes of action, but is well known to generate high levels of reactive oxygen species in cells which are believed to be causal in many of its biologic actions.1 ROS can both activate and suppress signaling through multiple intracellular pathways based on the amount and duration of ROS production.2 As the basal activity of the MEK1/2-ERK1/2 pathway is often high in acute myeloid leukemias, and that ATO is known to stimulate MEK1/2-ERK1/2 signaling in leukemia, the authors investigated whether knock down of the downstream effector of ERK1/2, RSK1, could enhance the anti-leukemic activity of ATO.3,4

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“…The effect of XAF1 on endothelial cell proliferation was evaluated using WST-1 assay as described previously [9] .…”

Section: Detection Of Ms1 Proliferation By Wst-1 Assaymentioning

confidence: 99%

XIAP-Associated Factor 1 (XAF1) Suppresses Angiogenesis in Mouse Endothelial Cells

Qiao¹,

Gu²,

Dai³

et al. 2008

Tumor Biol

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Objectives: XIAP-associated factor 1 (XAF1) is a tumor suppressor gene, but its role in angiogenesis is unknown. We investigated whether XAF1 has any antiangiogenesis effect. Methods: MS1 (a mouse endothelial cell line) was infected with an adenoviral vector ZD55-XAF1. Controls were uninfected or infected with ZD55-EGFP. Wound healing assay and tube formation assay were used to assess angiogenesis. Cell proliferation was detected by WST-1 assay, and apoptosis was detected by TUNEL and APOPercentage™ assays. Results: ZD55-XAF1 significantly upregulated XAF1, which was associated with decreased cell proliferation, migration and tube formation of MS1 cells. Ectopic overexpression of XAF1 induced apoptosis in MS1 and also sensitized cells to 5-fluorouracil-induced apoptosis. A significant decrease in the expression of Tie-1, Ang-1, Ang-2 and c-Myc was observed. Conclusions: Our data suggest that XAF1 possesses a potential antiangiogenesis effect. Suppressed expression of Tie-1, Ang-1, Ang-2 and c-Myc may be mechanistically responsible for the observed antiangiogenesis effect.

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NF-κB protects rat ARL-6 hepatocellular carcinoma cells against hydrogen peroxide-induced apoptosis

Cited by 12 publications

References 44 publications

Downregulation of hTERT: An Important As2O3 Induced Mechanism of Apoptosis in Myelodysplastic Syndrome

Downregulation of hTERT: An Important As2O3 Induced Mechanism of Apoptosis in Myelodysplastic Syndrome

Arsenic in leukemia

XIAP-Associated Factor 1 (XAF1) Suppresses Angiogenesis in Mouse Endothelial Cells

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