Dysregulation of TNFα-induced necroptotic signaling in chronic lymphocytic leukemia: suppression of CYLD gene by LEF1

Liu, Peng; Xu, Bei; Shen, Wenyi; Zhu, Heqin; Wu, Wei; Fu, Yuan; Chen, H; Dong, Han; Zhu, Yichao; Miao, Kou‐Rong; Xu, Wei; Li, J

doi:10.1038/leu.2011.357

Cited by 98 publications

(76 citation statements)

References 40 publications

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“…Liu et al reported that defects in apoptosis and necroptosis occurred simultaneously in CLL cells, and the expression levels of the two central members of the necroptosis pathway, RIP3 and CYLD, were significantly reduced in CLL cells. Co-stimulation by TNF-a and zVAD could not induce necroptosis in CLL cells, which suggested that the defect in necroptosis correlated with the pathogenesis of CLL [92]. These findings also demonstrated that the presence of normal necroptosis mechanisms is essential for the maintenance of normal hematopoiesis.…”

Section: Impact Of Tnf-a-mediated Necroptosis On Hematopoiesismentioning

confidence: 82%

TNF-α-induced programmed cell death in the pathogenesis of acquired aplastic anemia

Chen

Zou²,

et al. 2015

Expert Review of Hematology

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The mechanism of acquired aplastic anemia (AA), a bone marrow hematopoiesis failure disease, has not been fully understood. TNF-α is a pleiotropic cytokine involved in cell proliferation, differentiation and death, and inflammation through binding to specific receptors on cell membranes. Aberrant secretion of TNF-α contributes to a number of human diseases, including tumor development and inflammation. TNF-α is also an important negative regulator of hematopoiesis. Over-expression of TNF-α not only directly inhibits the proliferation and differentiation of hematopoietic cells, but also initiates the intracellular death pathway to induce hematopoietic cell death, leading to bone marrow hematopoiesis failure. In this review, we summarize the mechanisms underlying extrinsic apoptosis and necroptosis of hematopoietic cells induced by TNF-α, and discuss the role of TNF-α-induced programmed cell death in the pathogenesis of acquired AA.

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Section: Impact Of Tnf-a-mediated Necroptosis On Hematopoiesismentioning

confidence: 82%

TNF-α-induced programmed cell death in the pathogenesis of acquired aplastic anemia

Chen

Zou²,

et al. 2015

Expert Review of Hematology

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“…60 CYLD also serves as a regulator of necroptosis, an alternative cell death pathway when apoptotic pathways are suppressed or blocked. 61 Absence of CYLD is reported in many cancers 62 and CLL patients with high CYLD levels were reported to have improved overall survival. 60 IBTK is a physiologic inhibitor of BTK.…”

Section: Discussionmentioning

confidence: 98%

Ibrutinib downregulates a subset of miRNA leading to upregulation of tumor suppressors and inhibition of cell proliferation in chronic lymphocytic leukemia

et al. 2016

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The lymph node (LN) is the site of chronic lymphocytic leukemia (CLL) cell activation and proliferation. Aberrant microRNA (miRNA) expression has been shown to have a role in CLL pathogenesis; however, a comparison of miRNA expression between CLL cells in the LN and the peripheral blood (PB) has previously not been reported. On the basis of the analysis of 17 paired LN and PB samples from CLL patients, we identify a panel of miRNAs that are increased in LN CLL cells correlating with an activation phenotype. When evaluated in CLL cells from 38 patients pre and post treatment with ibrutinib, a subset of these miRNAs (miR-22, miR-34a, miR-146b and miR-181b) was significantly decreased in response to ibrutinib. A concomitant increase in putative miRNA target transcripts (ARID1B, ARID2, ATM, CYLD, FOXP1, HDAC1, IBTK, PTEN and SMAD4) was also observed. Functional studies confirmed targets of ibrutinib-responsive miRNAs to include messenger RNA transcripts of multiple tumor suppressors. Knockdown of endogenous miR-34a and miR146b resulted in increased transcription of tumor suppressors and inhibition of cell proliferation. These findings demonstrate that ibrutinib downregulates the expression of a subset of miRNAs related to B-cell activation leading to increased expression of miRNA targets including tumor suppressors and a reduction in cell proliferation.

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“…RIP3 has recently been outlined as a key gene involved in the regulation of apoptosis and necroptosis [13]. RIP3 was proved to play an important role in some malignant tumors, including hepatocarcinoma, chronic lymphocytic leukemia, osteosarcoma and glioblastoma [14][15][16][17]. However, the expression of RIP3 and its potential role in colorectal cancer remains elusive.…”

Section: Discussionmentioning

confidence: 99%

Receptor-interacting protein kinase 3 is a predictor of survival and plays a tumor suppressive role in colorectal cancer

Feng¹,

Song²,

Yu.Yu.³

et al. 2015

neo

124

102

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Receptor-interacting protein kinase 3 (RIP3) is a member of the RIP Ser/Thr kinase family, plays an important role in regulating cell survival, cell apoptosis and cell necrosis. However, the role of RIP3 in the carcinogenesis of colorectal cancer is still poorly understood.We used quantitative PCR and Western blot analysis to examine RIP3 expression in primary colorectal cancer and paired normal colorectal mucosa. RIP3 clinicopathological significance was assessed by immunohistochemical staining in 112 cases of primary colorectal cancer paired with noncancerous tissues. The biological function of RIP3 overexpression was measured by CCK8 assay and plate colony formation assay. Dual staining with fluorescent Annexin V and propidium iodide (PI) was used to discriminate apoptotic or necrotic cell death.RIP3 expression was significantly lower in colorectal cancer and associated with T stage, M stage and AJCC stage. Cox proportional hazard models showed that RIP3 expression was an independent prognostic factor for overall survival and disease-free survival in patients with colorectal cancer. Overexpression of RIP3 significantly suppressed the proliferation of colorectal cancer cells in vitro.Our results suggest that RIP3 may function as a novel prognostic indicator after surgery and play a suppressive role in the colorectal carcinogenesis.

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Dysregulation of TNFα-induced necroptotic signaling in chronic lymphocytic leukemia: suppression of CYLD gene by LEF1

Cited by 98 publications

References 40 publications

TNF-α-induced programmed cell death in the pathogenesis of acquired aplastic anemia

TNF-α-induced programmed cell death in the pathogenesis of acquired aplastic anemia

Ibrutinib downregulates a subset of miRNA leading to upregulation of tumor suppressors and inhibition of cell proliferation in chronic lymphocytic leukemia

Receptor-interacting protein kinase 3 is a predictor of survival and plays a tumor suppressive role in colorectal cancer

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