Interference with nuclear factor kappa B and c-Jun NH2-terminal kinase signaling by TRAF6C small interfering RNA inhibits myeloma cell proliferation and enhances apoptosis

H, Chen; Li, M; Campbell, Richard A.; Burkhardt, Kim; Zhu, Daocheng; Li, S G; Lee, H J; Wang, C; Zeng, Zhaohui; Gordon, Melinda S.; Bonavida, Benjamin; Berenson, James R.

doi:10.1038/sj.onc.1209653

Cited by 38 publications

(25 citation statements)

References 28 publications

(33 reference statements)

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“…Recent studies have shown that down-regulation of TRAF6 associated with NF-B inhibition blocks MM cell proliferation, 39 and that TAK-1 40 and RIP2 41 are upstream molecules of IKK. In our study, bortezomib significantly triggered phosphorylation of IKK␤ and its upstream RIP2, without alteration in TRAF6 protein or phosphorylation of TAK-1.…”

Section: Discussionmentioning

confidence: 99%

Bortezomib induces canonical nuclear factor-κB activation in multiple myeloma cells

Hideshima

Ikeda

Chauhan

et al. 2009

Blood

323

283

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Section: Discussionmentioning

confidence: 99%

Bortezomib induces canonical nuclear factor-κB activation in multiple myeloma cells

Hideshima

Ikeda

Chauhan

et al. 2009

Blood

323

283

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“…Moreover, the TNF-TNFR complex also leads to the recruitment of TRAF molecules that signal downstream, activating the transcription factors NF-B and JNK (138,139). Chandel et al suggest that TRAFs play an important role in regulating the increase of intracellular reactive oxygen species (ROS), and that TRAFs regulate the cellular redox status (140).…”

Section: Cross-linking Of Tnf and Tnfr Type I Dependent Pathwaymentioning

confidence: 99%

Cell Death Mechanisms Induced by Cytotoxic Lymphocytes

et al. 2009

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One of the functions of the immune system is to recognize and destroy abnormal or infected cells to maintain homeostasis. This is accomplished by cytotoxic lymphocytes. Cytotoxicity is a highly organized multifactor process. Here, we reviewed the apoptosis pathways induced by the two main cytotoxic lymphocyte subsets, natural killer (NK) cells and CD8 + T cells. In base to recent experimental evidence, we reviewed NK receptors involved in recognition of target-cell, as well as lytic molecules such as perforin, granzymes-A and -B, and granulysin. In addition, we reviewed the Fas-FasL intercellular linkage mediated pathway, and briefly the cross-linking of tumor necrosis factor (TNF) and TNF receptor pathway. We discussed three models of possible molecular interaction between lytic molecules from effector cytotoxic cells and target-cell membrane to induction of apoptosis. Cellular & Molecular Immunology. 2009;6(1):15-25.

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“…Using these stringent criteria, we found that the miR-135b and miR-146a (Table 3), both downregulated in MM with t(4;14), targeted two genes (PELI2 and IRAK1) involved in IL-1 signalling Table 4 Potential microRNA (miRNA)-mRNA interactions deregulated in the multiple myeloma (MM) with monosomy 13 as a unique abnormality pathway, which is a potent inducer of IL-6. IRAK1 (IL-1 receptor-associated kinase) activates and recruits TRAF6 to the IL-1 receptor complex, 45,46 and PELI2 is a scaffold protein probably involved in the IL-1 signalling through its interaction with the complex containing IRAK kinases and TRAF6. 47 Both IRAK1 and PELI2 display two matches to the miR-146a and miR-135b respectively, which increases the prediction specificity.…”

Section: Tablementioning

confidence: 99%

Deregulation of microRNA expression in the different genetic subtypes of multiple myeloma and correlation with gene expression profiling

et al. 2010

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Specific microRNA (miRNA) signatures have been associated with different cytogenetic subtypes in acute leukemias. This finding prompted us to investigate potential associations between genetic abnormalities in multiple myeloma (MM) and singular miRNA expression profiles. Moreover, global gene expression profiling was also analyzed to find correlated miRNA gene expression and select miRNA target genes that show such correlation. For this purpose, we analyzed the expression level of 365 miRNAs and the gene expression profiling in 60 newly diagnosed MM patients, selected to represent the most relevant recurrent genetic abnormalities. Supervised analysis showed significantly deregulated miRNAs in the different cytogenetic subtypes as compared with normal PC. It is interesting to note that miR-1 and miR-133a clustered on the same chromosomal loci, were specifically overexpressed in the cases with t(14;16). The analysis of the relationship between miRNA expression and their respective target genes showed a conserved inverse correlation between several miRNAs deregulated in MM cells and CCND2 expression level. These results illustrate, for the first time, that miRNA expression pattern in MM is associated with genetic abnormalities, and that the correlation of the expression profile of miRNA and their putative mRNA targets is useful to find statistically significant protein-coding genes in MM pathogenesis associated with changes in specific miRNAs.

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Interference with nuclear factor kappa B and c-Jun NH2-terminal kinase signaling by TRAF6C small interfering RNA inhibits myeloma cell proliferation and enhances apoptosis

Cited by 38 publications

References 28 publications

Bortezomib induces canonical nuclear factor-κB activation in multiple myeloma cells

Bortezomib induces canonical nuclear factor-κB activation in multiple myeloma cells

Cell Death Mechanisms Induced by Cytotoxic Lymphocytes

Deregulation of microRNA expression in the different genetic subtypes of multiple myeloma and correlation with gene expression profiling

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