Increased Ras Expression and Caspase-Independent Neuroblastoma Cell Death: Possible Mechanism of Spontaneous Neuroblastoma Regression

Kitanaka, Chifumi; Kato, Keisuke; Ijiri, Rieko; Sakurada, Kaori; Tomiyama, Arata; Noguchi, Kohji; Nagashima, Youji; Nakagawara, Akira; Momoi, Takashi; Toyoda, Yasunori; Kigasawa, Hisato; Nishi, Toshiji; Shirouzu, Mikako; Yokoyama, Shigeyuki; Tanaka, Yukichi; Kuchino, Yoshiyuki

doi:10.1093/jnci/94.5.358

Cited by 105 publications

(86 citation statements)

References 32 publications

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“…Similarly, Ras triggers autophagic cell death in neuroblastoma, causing tumor regression (40). Importantly, drug-induced autophagy causes K-Ras degradation and cell death in multiple tumors (41).…”

Section: Discussionmentioning

confidence: 99%

Transcriptional Repressor DAXX Promotes Prostate Cancer Tumorigenicity via Suppression of Autophagy

Puto

Brognard

Hunter

2015

Journal of Biological Chemistry

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Background: Transcriptional repressor DAXX suppresses several tumor suppressor genes and is up-regulated in many cancers. Results: We demonstrate that DAXX has potent growth-enhancing effects on primary prostatic malignancy through inhibition of autophagy. Conclusion: In the early stages of tumorigenesis, autophagy suppresses prostate tumor formation. Significance: This is the first study to link prostate cancer development to autophagy suppression by DAXX.

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Section: Discussionmentioning

confidence: 99%

Transcriptional Repressor DAXX Promotes Prostate Cancer Tumorigenicity via Suppression of Autophagy

Puto

Brognard

Hunter

2015

Journal of Biological Chemistry

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“…Expression levels of NEDL1 were higher in favorable neuroblastoma than those in unfavorable neuroblastoma. Favorable neuroblastoma undergoes spontaneous regression through NEDL1 cooperates with p53 to induce apoptosis Y Li et al apoptosis and/or neuronal differentiation (Kitanaka et al, 2002). In contrast to other human tumors, p53 is rarely mutated in neuroblastoma (Moll et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

A novel HECT-type E3 ubiquitin protein ligase NEDL1 enhances the p53-mediated apoptotic cell death in its catalytic activity-independent manner

Ozaki

Kikuchi

et al. 2008

Oncogene

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NEDL1 (NEDD4-like ubiquitin protein ligase-1) is a newly identified HECT-type E3 ubiquitin protein ligase highly expressed in favorable neuroblastomas as compared with unfavorable ones. In this study, we found that NEDL1 cooperates with p53 to induce apoptosis. During cisplatin (CDDP)-mediated apoptosis in neuroblastoma SH-SY5Y cells, p53 was induced to accumulate in association with an increase in expression levels of NEDL1. Enforced expression of NEDL1 resulted in a decrease in number of G418-resistant colonies in SH-SY5Y and U2OS cells bearing wild-type p53, whereas NEDL1 had undetectable effect on p53-deficient H1299 and SAOS-2 cells. Similarly, enforced expression of NEDL1 increased number of U2OS cells with sub-G1 DNA content. Co-immunoprecipitation and in vitro binding assays revealed that NEDL1 binds to the COOH-terminal region of p53. Luciferase reporter assay showed that NEDL1 has an ability to enhance the transcriptional activity of p53. Small interfering RNAmediated knockdown of the endogenous NEDL1 conferred the resistance of U2OS cells to adriamycin. It is noteworthy that NEDL1 enhanced pro-apoptotic activity of p53 in its catalytic activity-independent manner. Taken together, our present findings suggest that functional interaction of NEDL1 with p53 might contribute to the induction of apoptosis in cancerous cells bearing wildtype p53.

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“…pGEX2T-c-Myc(1-262), pGEX2T-Pim1, and pGEX2T-Cdc25A, pGEX4T-c-Jun(1-92), pcDNA3EGFP have been described previously. [39][40][41] pGEX2T-c-Myc (full-length) was constructed by subcloning into pGEX2T a cDNA fragment containing the entire coding region of human c-myc in frame to GST. pcDNA3-mBcl-xL and pGEX2T-mBcl-xL are gifts from Dr. Yoshihide Tsujimoto (Osaka University Medical School) and express mouse Bcl-xL in mammalian cells and mouse Bcl-xL fused to GST in Escherichia coli, respectively.…”

Section: Methodsmentioning

confidence: 99%

Physical and functional interaction between BH3-only protein Hrk and mitochondrial pore-forming protein p32

Sunayama

Ando²,

Itoh³

et al. 2004

Cell Death Differ

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Bcl-2 homology domain (BH) 3-only proteins of the proapoptotic Bcl-2 subfamily play a key role as initiators of mitochondria-dependent apoptosis. To date, at least 10 mammalian BH3-only proteins have been identified, and it is now being realized that they have different roles and mechanisms of regulation in the transduction of apoptotic signals to mitochondria. Hrk/DP5 is one of the mammalian BH3-only proteins implicated in a variety of physiological and pathological apoptosis, yet the molecular mechanism involved in Hrk-mediated apoptosis remains poorly understood. In an attempt to identify cellular proteins participating in Hrkmediated apoptosis, we have conducted yeast two-hybrid screening for Hrk-interacting proteins and isolated p32, a mitochondrial protein that has been shown to form a channel consisting of its homotrimer. In vitro binding, co-immunoprecipitation, as well as immunocytochemical analyses verified specific interaction and colocalization of Hrk and p32, both of which depended on the presence of the highly conserved C-terminal region of p32. Importantly, Hrk-induced apoptosis was suppressed by the expression of p32 mutants lacking the N-terminal mitochondrial signal sequence (p32 (74-282)) and the conserved C-terminal region (p32 (1-221)), which are expected to inhibit binding of Hrk competitively to the endogenous p32 protein and to disrupt the channel function of p32, respectively. Furthermore, small interfering RNA-mediated knockdown of p32 conferred protection against Hrk-induced apoptosis. Altogether, these results suggest that p32 may be a key molecule that links Hrk to mitochondria and is critically involved in the regulation of Hrk-mediated apoptosis.

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Increased Ras Expression and Caspase-Independent Neuroblastoma Cell Death: Possible Mechanism of Spontaneous Neuroblastoma Regression

Abstract: High-level expression of H-Ras in neuroblastoma cells is associated with caspase cascade-independent, nonapoptotic PCD. This Ras-mediated nonapoptotic tumor cell death may play a key role in spontaneous regression of neuroblastoma.

Cited by 105 publications

References 32 publications

Transcriptional Repressor DAXX Promotes Prostate Cancer Tumorigenicity via Suppression of Autophagy

Transcriptional Repressor DAXX Promotes Prostate Cancer Tumorigenicity via Suppression of Autophagy

A novel HECT-type E3 ubiquitin protein ligase NEDL1 enhances the p53-mediated apoptotic cell death in its catalytic activity-independent manner

Physical and functional interaction between BH3-only protein Hrk and mitochondrial pore-forming protein p32

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