Autocrine TNFalpha signaling renders human cancer cells susceptible to Smac-mimetic-induced apoptosis.

By S. Petersen, Lai Wang, Asligul Yalcin-Chin, Lin Li, M. Peyton, J. Minna, P. Harran, Xiaodong Wang. Cancer Cell, 2007

606 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/05d57aba25b455589dc450c48d921bffd416e9b9

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. V. Bhoj
2. Zhijian J. Chen
3. P. Meier
4. G. Gores
5. D. Vučić
6. Simone Fulda
7. F. Balkwill
8. N. Perkins

In Immunology

1. Zhijian J. Chen
2. Fenghe Du
3. V. Bhoj
4. P. Meier
5. G. Gores
6. D. Vučić
7. Simone Fulda
8. F. Balkwill

In Molecular Biology

1. Zhijian J. Chen
2. D. Vučić
3. Simone Fulda
4. Fenghe Du
5. V. Bhoj
6. P. Meier
7. Xiaodong Wang
8. G. Gores

Citations in the corpus

• Life and death by death receptors (2009, background): “Furthermore, in the absence of c-IAP1/2 (cellular inhibitor of apoptosis 1/2), death receptors such as TNF-R1 (vide infra) can signal cell death despite NF- B activation (110).”
• Targeting IAP proteins for therapeutic intervention in cancer (2012, background): “However, the most striking feature of bivalent antagonists is their high potency in cell death assays and tumour growth inhibition assay”
• cIAP1 and cIAP2 facilitate cancer cell survival by functioning as E3 ligases that promote RIP1 ubiquitination. (2008, result): “This work complements and extends data from several recent papers published after the submission of this manuscript (Gaither et al., 2007; Petersen et al., 2007; Varfolomeev et al., 2007; Vince et al., 2007).”
• Ubiquitylation in innate and adaptive immunity (2009, background): “The binding of SMAC, or small-molecule SMAC mimetics, to cIAPs induces the dimerization, autoubiquitylation and proteasomal degradation of these ubiquitin ligase”
• The Ripoptosome, a signaling platform that assembles in response to genotoxic stress and loss of IAPs. (2011, background): “…cells die upon cIAP depletion because loss of cIAPs results in enhanced sensitivity to autocrine TNF. ‘‘SM-resistant’’ cells stay alive because they do not produce TNF (Cheung et al., 2009; Petersen et al., 2007). cIAP depletion also occurs in response to genotoxic stress (Yang et al., 2000).”
• Tumour necrosis factor and cancer (2009, background): “SMAC (also known as DIABLO) mimetic drugs switch off the survival and inflammatory pathways that are normally induced by autocrine TNF ( Box 2 ), causing those cancer cell lines that produce TNF to self-destruc”
• Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. (2009, background): “A Smac Mimetic Plus a Pan-Caspase Inhibitor Induce Necrosis in HT-29 Cells Smac mimetics have been shown to induce apoptosis in certain tumor cell lines (Petersen et al., 2007; Vince et al., 2007; Varfolomeev et al., 2007), and death can be completely blocked with a pan-caspase inhibitor, z-VAD.”