2009
DOI: 10.1073/pnas.0902880106
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Inhibition of Hsp90 via 17-DMAG induces apoptosis in a p53-dependent manner to prevent medulloblastoma

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Cited by 30 publications
(30 citation statements)
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“…Activation of macrophages and monocytes in inflammation can prevent apoptosis and lead to prolonged macrophage and monocyte viability [37,38]. Apoptosis induced by HSP90 inhibitors has shown selectivity for abnormal cells, and recently was shown to be dependent on the activation of specific apoptotic proteins [39]. The HSP90 inhibitor 17-DMAG has been shown to induce apoptosis selectively in chronic lymphoid leukemia cells [19].…”
Section: Discussionmentioning
confidence: 99%
“…Activation of macrophages and monocytes in inflammation can prevent apoptosis and lead to prolonged macrophage and monocyte viability [37,38]. Apoptosis induced by HSP90 inhibitors has shown selectivity for abnormal cells, and recently was shown to be dependent on the activation of specific apoptotic proteins [39]. The HSP90 inhibitor 17-DMAG has been shown to induce apoptosis selectively in chronic lymphoid leukemia cells [19].…”
Section: Discussionmentioning
confidence: 99%
“…14,18 In studying MBs, Ayrault et al reported that, in order for 17-DMAG to exert its antitumorigenic effect, an intact p53 response is required. 2 Apart from HSP90, an HSP70 inhibitor has also been developed and showed promise as an anticancer compound. 3 The increased expression of both HSP70 and HSP90-α in the present study suggests a possible therapeutic implication in MB.…”
mentioning
confidence: 99%
“…These effects were attributed to the degradation of the Hsp90 clients, which are driver oncoproteins in these tumor types. Studies by us and other groups showed that p53 mutational status influences 17-AAG sensitivity through the effects on p53 downstream targets including PUMA, Bax, Bim, and p21 (1315). Our recent study showed that colon cancer cells contain a small fraction (~0.1%) of pre-existing FWB7 -mutant cells, which can be enriched upon treatment with the multi-kinase inhibitor regorafenib, leading to acquired drug resistance (29).…”
Section: Discussionmentioning
confidence: 88%
“…Previous studies showed that geldanamycin and 17-AAG induce apoptosis and inhibit tumor metastasis and angiogenesis (2, 9). Several anticancer mechanisms of Hsp90 inhibitors have been proposed, such as downregulation of Akt (10), inhibition of NF-kB activation due to IKK destabilization (11), endoplasmic reticulum stress (12), and more recently, activation of p53 and its downstream targets (1315). However, the mechanisms by which Hsp90 inhibitors selectively kill tumor cells are still not well understood.…”
Section: Introductionmentioning
confidence: 99%