A novel apoptotic pathway induced by the drs tumor suppressor gene

Tambe, Yukihiro; Isono, Takahiro; Haraguchi, Satoru; Yoshioka-Yamashita, Atsuko; Yutsudo, Masuo; Inoue, Hirokazu

doi:10.1038/sj.onc.1207419

Cited by 43 publications

(43 citation statements)

References 37 publications

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“…The deletion of these repeats apparently decreased apoptosis, indicating that sushi domains may be the key functional domains in apoptosis; however, the binding partners of sushi domain are unknown. Drs-induced apoptosis involved sequential activation of caspases 12, 9, and 3; however, neither cytochrome-c release nor activation of caspase 8 was observed, suggesting that mitochondrial pathway does not mediate drs-induced apoptosis (22). In contrast, in the present study, TMPS activated not only caspase 9 and 3 but also caspase 8, indicating that TMPSinduced apoptosis may involve the participation of various kinds of apoptotic pathways.…”

Section: Discussioncontrasting

confidence: 52%

Regulation of apoptosis by p53-inducible transmembrane protein containing sushi domain

Arakara¹

2010

Oncol Rep

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Abstract. The tumor suppressor p53 is a transcription factor that induces the transcription of various target genes in response to DNA damage and it protects the cells from malignant transformation. In this study, we performed cDNA microarray analysis and found that the transmembrane protein containing sushi domain (TMPS) gene, which encodes a putative type I transmembrane protein, is a novel p53-target gene. TMPS contains a sushi domain in the extracellular region, which is associated with protein-protein interaction. TMPS expression is induced by endogenous p53 under genotoxic stress in several cancer cell lines. Reporter assay revealed p53-dependent transactivation of the p53 binding-sites (BSs) located in the intron 1 of TMPS. Chromatin immunoprecipitation (ChIP) assay showed that p53 binds to these BSs in vivo. Overexpression of TMPS induced apoptosis through the activation of caspase-3, 8, and 9 in various cancer cell lines. Moreover, Á-irradiation induced the expression of TMPS mRNA in the spleen and colon of p53 +/+ mice but not in those of p53 -/-mice. These data indicate that TMPS may play a role in p53-dependent apoptosis under DNA damage condition.

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Section: Discussioncontrasting

confidence: 52%

Regulation of apoptosis by p53-inducible transmembrane protein containing sushi domain

Arakara¹

2010

Oncol Rep

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“…Tambe Y et al [7] also showed that the product of drs gene can interact with Nogo-B, and the coexpression of drs and Nogo-B can increase the efficiency of apoptosis. Previous experiments demonstrate that overexpressed Nogo-B protein induces apoptosis in various cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor

et al. 2007

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Objective Nogo-A is an axon regeneration inhibitor, and its function in central nervous system (CNS) is still unknown. The present study is to explore the relationship between the expression of Nogo-A and the malignancy of oligodendroglial tumors in patients. Methods Tumor tissue samples with different malignancy grade were obtained from the hospitals. The samples used for detection had been diagnosed as oligodendroglial tumors (oligodendroglioma or anaplastic oligodendroglioma). The expression of Nogo-A was detected by immunohistochemistry and western-blot analysis. The correlation test between the Nogo-A expression and the morphological changes (the percentages of atypical cells and mitotic cells in the tumors) related to the malignancy of tumor tissues was performed. Results There was significant negative correlation between the Nogo-A expression and the morphological change of tumor tissues according to immunohistochemistry. Western-blot analysis also indicated that the gray value of Nogo-A protein band in the oligodendroglioma group was significantly higher than that in the anaplastic oligodendroglioma group. Conclusion Nogo-A expression was negatively correlated with the malignancy grade of oligodendroglial tumors.

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“…Seven of the 17 highly upregulated genes in the HGG-02 cells represent well accepted or potential tumor suppressors, including CDKN2A (35,36), TFAP2C (37), IGFBP3 (38), CDKN2B (36), FRZB (39), SRPX (40) and Siva1 (41). However, the downregulated genes involved genes associated with the ECM, including COL6A3, COL1A1, DCN, FN1 and FBN1.…”

Section: Discussionmentioning

confidence: 99%

EGFR signaling in the HGG-02 glioblastoma cell line with an unusual loss of EGFR gene copy

et al. 2013

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Abstract. Epidermal growth factor receptor (EGFR) gene amplification and the overexpression of EGFR are described as common features of glioblastoma multiforme (GBM). Nevertheless, we previously reported the loss of EGFR gene copy in a GBM specimen from a patient with an unusually favorable course of the disease, and the HGG-02 cell line with this aberration was successfully derived from this tumor. Here, we present a detailed analysis of changes in gene expression and cell signaling in the HGG-02 cell line; the GM7 reference cell line with a standard EGFR gene copy number derived from a very aggressive GBM was used as a control. We confirmed the downregulation of EGFR expression and signaling in HGG-02 cells using different methods (RTK analysis, gene profiling and RT-PCR). Other changes that may have contributed to the non-aggressive phenotype of the primary tumor were identified, including the downregulated phosphorylation of the Axl and Trk receptors, as well as increased activity of JNK and p38 kinases. Notably, differences in PDGF signaling were detected in both of these cell lines; HGG-02 cells preferentially expressed and signaled through PDGFRα, and PDGFRβ was strongly overexpressed and phosphorylated in the GM7 reference cell line. Using expression profiling of cancer-related genes, we revealed the specific profile of HGG-02 cells that included upregulated tumor-suppressors as well as downregulated genes associated with the extracellular matrix. This study represents the first comprehensive analysis of gene expression and cell signaling in glioblastoma cells with lower EGFR gene

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A novel apoptotic pathway induced by the drs tumor suppressor gene

Cited by 43 publications

References 37 publications

Regulation of apoptosis by p53-inducible transmembrane protein containing sushi domain

Regulation of apoptosis by p53-inducible transmembrane protein containing sushi domain

Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor

EGFR signaling in the HGG-02 glioblastoma cell line with an unusual loss of EGFR gene copy

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