TNF Signaling through RIP1 Kinase Enhances SN38-Induced Death in Colon Adenocarcinoma

Cabal-Hierro, Lucía; O’Dwyer, Peter J.

doi:10.1158/1541-7786.mcr-16-0329

Cited by 18 publications

(19 citation statements)

References 48 publications

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“…In particular, 12 of the 31 identified genes have been reported in the literatures to be related to colon cancer recurrence [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37], which can be regarded as validation to our prediction results for these 12 genes. For the other 19 genes identified by us, we cannot exclude the possibility that some of them are due to false positive prediction.…”

Section: Discussionmentioning

confidence: 54%

Exploration of immunogene in colon cancer recurrence

Sun¹,

Yao²,

Yuan³

et al. 2018

Oncotarget

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Colon adenocarcinoma is the third most common cancer with high risk of recurrence and deteriorative consequences. Given the importance of immune genes in tumor regulation and cancer immunotherapy, there is a need to comprehensively profile the immunoregulatory genes from multiple types of colon cancer patient genomic data for discovering important associations and potential therapeutic targets of colon cancer recurrence. We used publicly available colon tumor tissue genomic data from The Cancer Genome Atlas database and immune genes data from innateDB database in this study. We derived the immune genes profiles by exploring multiple genomic profiles (gene expression, clinical and somatic mutation) in colon cancer. Some of the synthetic lethal genes we identified, such as CASP14, MS4A6E, KIR2DL1, KIR3DL1, KIR2DL3, CCL1, IL36B, FOXO3, POU2F1, SMAD3, HOXA9, PACS1, PROM1, DIDO1, SRC, CBFA2T2, NCOA6, PGAM1 and PROC, have been suggested to be potential targets correlated with immune genes for colon cancer recurrence treatment. Moreover, TLR2 could be promisingly new early stage indicator for colon adenocarcinoma recurrence. This is a systematic study that combines three different types of genomic data to molecularly characterize colon cancer and aims to identify potential targets for colon adenocarcinoma therapy. Meanwhile, the integrative analysis of immune genes for colon cancer could assist in identifying potential new symbols for colon adenocarcinoma recurrence.

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Section: Discussionmentioning

confidence: 54%

Exploration of immunogene in colon cancer recurrence

Sun¹,

Yao²,

Yuan³

et al. 2018

Oncotarget

View full text Add to dashboard Cite

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“…Previous studies have indicated that increased RIP3 expression was correlated with cancer development, including colon and lung cancers, nasopharyngeal carcinoma and non-Hodgkin lymphoma (120-122). The topoisomerase inhibitor SN38, an active metabolite of irinotecan, was demonstrated to mediate cytotoxicity through the TNF/TNFR signaling pathway in a panel of colon cancer cells (123). SN38 also promoted the progression of necroptosis, inhibited cell proliferation and induced DNA damage accumulation (123).…”

Section: Application Potential Of Rip1/rip3 Inhibition In Disease mentioning

confidence: 99%

“…The topoisomerase inhibitor SN38, an active metabolite of irinotecan, was demonstrated to mediate cytotoxicity through the TNF/TNFR signaling pathway in a panel of colon cancer cells (123). SN38 also promoted the progression of necroptosis, inhibited cell proliferation and induced DNA damage accumulation (123). This suggested that the SN38-induced activation of RIP1 and subsequent necroptosis may exert the therapeutic efficacy on colorectal carcinoma (123).…”

Section: Application Potential Of Rip1/rip3 Inhibition In Disease mentioning

confidence: 99%

“…SN38 also promoted the progression of necroptosis, inhibited cell proliferation and induced DNA damage accumulation (123). This suggested that the SN38-induced activation of RIP1 and subsequent necroptosis may exert the therapeutic efficacy on colorectal carcinoma (123). Furthermore, Xin et al (124) reported that degradation of suppressor of cytokine signaling 1, a key negative regulator of IFN-γ signaling, was prevented by TNF through RIP1/RIP3 signaling.…”

Section: Application Potential Of Rip1/rip3 Inhibition In Disease mentioning

confidence: 99%

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RIP1/RIP3-regulated necroptosis as a target for multifaceted disease therapy (Review)

et al. 2019

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Necroptosis is a type of programmed cell death with necrotic morphology, occurring in a variety of biological processes, including inflammation, immune response, embryonic development and metabolic abnormalities. The current nomenclature defines necroptosis as cell death mediated by signal transduction from receptor-interacting serine/threonine kinase (RIP) 1 to RIP3 (hereafter called RIP1/RIP3). However, RIP3-dependent cell death would be a more precise definition of necroptosis. RIP3 is indispensable for necroptosis, while RIP1 is not consistently involved in the signal transduction. Notably, deletion of RIP1 even promotes RIP3-mediated necroptosis under certain conditions. Necroptosis was previously thought as an alternate process of cell death in case of apoptosis inhibition. Currently, necroptosis is recognized to serve a pivotal role in regulating various physiological processes. Of note, it mediates a variety of human diseases, such as ischemic brain injury, immune system disorders and cancer. Targeting and inhibiting necroptosis, therefore, has the potential to be used for therapeutic purposes. To date, research has elucidated the suppression of RIP1/RIP3 via effective inhibitors and highlighted their potential application in disease therapy. The present review focused on the molecular mechanisms of RIP1/RIP3-mediated necroptosis, explored the functions of RIP1/RIP3 in necroptosis, discussed their potential as a novel therapeutic target for disease therapy, and provided valuable suggestions for further study in this field.

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“…The topoisomerase inhibitor SN38, an active metabolite of irinotecan, causes cytotoxicity through the TNF/TNFR signaling pathway in a panel of colon cancer cells and promotes the progression of necroptosis, [ 123 ], suggesting its potential use in the treatment of CRC [ 157 ].…”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

Necroptosis in Intestinal Inflammation and Cancer: New Concepts and Therapeutic Perspectives

et al. 2020

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Necroptosis is a caspases-independent programmed cell death displaying intermediate features between necrosis and apoptosis. Albeit some physiological roles during embryonic development such tissue homeostasis and innate immune response are documented, necroptosis is mainly considered a pro-inflammatory cell death. Key actors of necroptosis are the receptor-interacting-protein-kinases, RIPK1 and RIPK3, and their target, the mixed-lineage-kinase-domain-like protein, MLKL. The intestinal epithelium has one of the highest rates of cellular turnover in a process that is tightly regulated. Altered necroptosis at the intestinal epithelium leads to uncontrolled microbial translocation and deleterious inflammation. Indeed, necroptosis plays a role in many disease conditions and inhibiting necroptosis is currently considered a promising therapeutic strategy. In this review, we focus on the molecular mechanisms of necroptosis as well as its involvement in human diseases. We also discuss the present developing therapies that target necroptosis machinery.

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TNF Signaling through RIP1 Kinase Enhances SN38-Induced Death in Colon Adenocarcinoma

Cited by 18 publications

References 48 publications

Exploration of immunogene in colon cancer recurrence

Exploration of immunogene in colon cancer recurrence

RIP1/RIP3-regulated necroptosis as a target for multifaceted disease therapy (Review)

Necroptosis in Intestinal Inflammation and Cancer: New Concepts and Therapeutic Perspectives

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