2002
DOI: 10.1074/jbc.m207836200
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Arsenic Trioxide Promotes Histone H3 Phosphoacetylation at the Chromatin of CASPASE-10 in Acute Promyelocytic Leukemia Cells

Abstract: Arsenic trioxide (As 2 O 3 ) is highly effective for the treatment of acute promyelocytic leukemia, even in patients who are unresponsive to all-trans-retinoic acid therapy. As 2 O 3 is believed to function primarily by promoting apoptosis, but the underlying molecular mechanisms remain largely unknown. In this report, using cDNA arrays, we have examined the changes in gene expression profiles triggered by clinically achievable doses of As 2 O 3 in acute promyelocytic leukemia NB4 cells. CASPASE-10 expression … Show more

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Cited by 94 publications
(71 citation statements)
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References 38 publications
(60 reference statements)
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“…Arsenic trioxide (As 2 O 3 ) upregulates casp-10 gene expression but the role of this event in As 2 O 3 -induced apoptosis remains unknown (Li et al, 2002). A caspase-10 requirement for chemotherapy-induced apoptosis has (b) HeLa, 293T and U937 cells were left untreated or treated with 4 mM As 2 O 3 for 48 h before immunoblot analysis of procaspase-9 (proC9) and -10 (proC10).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Arsenic trioxide (As 2 O 3 ) upregulates casp-10 gene expression but the role of this event in As 2 O 3 -induced apoptosis remains unknown (Li et al, 2002). A caspase-10 requirement for chemotherapy-induced apoptosis has (b) HeLa, 293T and U937 cells were left untreated or treated with 4 mM As 2 O 3 for 48 h before immunoblot analysis of procaspase-9 (proC9) and -10 (proC10).…”
Section: Discussionmentioning
confidence: 99%
“…Chemotherapeutic agents such as etoposide and doxorubicin induce casp-10 gene transcription in a p53-dependent manner (Rikhof et al, 2003) and arsenic trioxide stimulates casp-10 gene transcription by promoting histone H3 phosphoacetylation in acute promyelocytic leukemia cells (Li et al, 2002). Recently, caspase-10 was shown to play a role in apoptosis induced by an anticancer drug, that is, paclitaxel, through a FADD-dependent mechanism (Park et al, 2004).…”
Section: Introductionmentioning
confidence: 99%
“…Although the mechanisms underlying most of the effects of As 2 O 3 are still not well understood, it is well established that As 2 O 3 is an oxidative stress agent (Kitchin and Ahmad, 2003), which, through the production of reactive oxygen species and the modification of thiol groups, induces protein and DNA damages (Meriin et al, 1999;Kapahi et al, 2000;Huang et al, 2004;Shi et al, 2004). These oxidative effects of As 2 O 3 result in the disruption of key signal transduction pathways, leading to the induction of apoptosis (Li et al, 2002). Indeed, As 2 O 3 activates the MAPK signaling pathways (Cavigelli et al, 1996;Meriin et al, 1999;Verma et al, 2002) and therefore induces the phosphorylation of a subset of transcription factors (AP-1, Elk, ATF2, CREB and others) (Bebien et al, 2003), PML (Hayakawa and Privalsky, 2004) and histones (Li et al, 2002(Li et al, , 2003aHe et al, 2003).…”
Section: Introductionmentioning
confidence: 99%
“…These oxidative effects of As 2 O 3 result in the disruption of key signal transduction pathways, leading to the induction of apoptosis (Li et al, 2002). Indeed, As 2 O 3 activates the MAPK signaling pathways (Cavigelli et al, 1996;Meriin et al, 1999;Verma et al, 2002) and therefore induces the phosphorylation of a subset of transcription factors (AP-1, Elk, ATF2, CREB and others) (Bebien et al, 2003), PML (Hayakawa and Privalsky, 2004) and histones (Li et al, 2002(Li et al, , 2003aHe et al, 2003). This leads to the increased transcription of critical apoptosisand proliferation-associated genes including among others, the proto-oncogenes c-fos, c-jun and Egr-1 (Lim et al, 1998;Bernstam and Nriagu, 2000;Liu et al, 2003) and caspases (Li et al, 2002).…”
Section: Introductionmentioning
confidence: 99%
“…A number of studies have demonstrated that iAs exposure induces global and gene-specific post-translational histone modifications such as reduction of acetylation in histone H3 and H4: loss of H4Lys 16 10 and H2AX phosphorylation, and decreases in H2B ubiquitination (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26).…”
mentioning
confidence: 99%