RIP3 overexpression sensitizes human breast cancer cells to parthenolide in vitro via intracellular ROS accumulation

Lü, Can; Zhou, Li; Xu, Hui; Chen, Xing Yu; Tong, Zhong Sheng; Liu, Xiao Dong; Jia, Yong; Chen, Yue

doi:10.1038/aps.2014.31

Cited by 13 publications

(8 citation statements)

References 32 publications

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“…1 a). Parthenolide, which can induce cell necrosis through reactive oxygen species (ROS) generation, was used as a positive control in the in vivo test [ 9 , 14 , 15 ]. After administration (i.p.)…”

Section: Resultsmentioning

confidence: 99%

Resibufogenin suppresses colorectal cancer growth and metastasis through RIP3-mediated necroptosis

Han

Wang

et al. 2018

J Transl Med

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BackgroundNecroptotic susceptibility is probably an intrinsic weakness of cancer. Here, we report that resibufogenin, a member of bufadienolide family, suppresses the growth and metastasis of colorectal cancer (CRC) through induction of necroptosis in vivo.MethodsSW480 cells with stably expressing enhanced green fluorescence protein were xenografted to BALB/c-nu mice to observe the growth of tumors. Liver metastasis was observed by injection of MC38 cells beneath the splenic capsule of mice. Protein expression was determined by immunohistochemistry, immunofluorescence and western blot.ResultsConsolidated in vitro results indicate that resibufogenin has anti-proliferative activity on CRC cells. PI staining and transmission electron microscope imaging suggest that the cell death induced by resibufogenin are mainly through necrosis, which is further confirmed by the ineffectiveness of z-VAD, a pan-caspase general inhibitor. In particular, resibufogenin induced necrosis is substantially abrogated in receptor-interacting protein kinase 3 (RIPK3) knockout mouse embryo fibroblasts. The RIP3-dependent necrosis has been classified as necroptosis. Resibufogenin triggeres necroptosis through upregulating RIP3 and phosphorylating mixed lineage kinase domain-like protein at Ser358. Resibufogenin also activates the expression of PYGL, GLUD1 and GLUL in a RIP3-dependent manner. Resibufogenin exerts cytotoxic effect by inducing reactive oxygen species accumulation which can be neutralized by N-acetylcysteine. Remarkably, resibufogenin significantly suppresses liver-metastasis from spleen implantation. The anti-neoplastic effect of this compound can be abrogated by RIP3 knockdown.ConclusionResibufogenin suppresses growth and metastasis of CRC through RIP3-mediated necroptosis.Electronic supplementary materialThe online version of this article (10.1186/s12967-018-1580-x) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Resibufogenin suppresses colorectal cancer growth and metastasis through RIP3-mediated necroptosis

Han

Wang

et al. 2018

J Transl Med

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“…The interaction of parthenolide with the plasma membrane led to membrane rupture and resulted in rapid necrotic cell death [ 308 ]. Intriguingly, parthenolide-mediated necrosis in human breast cancer MDA-MB231 cells was reduced by NAC and NEC-1, implying the role for activation of ROS and RIPK-1 in these processes [ 309 ]. Furthermore, parthenolide was found to inhibit the NF-κB activity associated with necrosis in multiple myeloma via targeting TNF receptor associated factor (TRAF)-6, as indicated in [ 310 ].…”

Section: Necroptosis Signaling Pathways Cancer and Natural Compoundsmentioning

confidence: 99%

Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells

Guamán-Ortiz

Orellana²,

Ratovitski³

2017

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Cell death is an innate capability of cells to be removed from microenvironment, if and when they are damaged by multiple stresses. Cell death is often regulated by multiple molecular pathways and mechanism, including apoptosis, autophagy, and necroptosis. The molecular network underlying these processes is often intertwined and one pathway can dynamically shift to another one acquiring certain protein components, in particular upon treatment with various drugs. The strategy to treat human cancer ultimately relies on the ability of anticancer therapeutics to induce tumor-specific cell death, while leaving normal adjacent cells undamaged. However, tumor cells often develop the resistance to the drug-induced cell death, thus representing a great challenge for the anticancer approaches. Numerous compounds originated from the natural sources and biopharmaceutical industries are applied today in clinics showing advantageous results. However, some exhibit serious toxic side effects. Thus, novel effective therapeutic approaches in treating cancers are continued to be developed. Natural compounds with anticancer activity have gained a great interest among researchers and clinicians alike since they have shown more favorable safety and efficacy then the synthetic marketed drugs. Numerous studies in vitro and in vivo have found that several natural compounds display promising anticancer potentials. This review underlines certain information regarding the role of natural compounds from plants, microorganisms and sea life forms, which are able to induce non-apoptotic cell death in tumor cells, namely autophagy and necroptosis.

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“…In ischemia-reperfusion injury, NF-κB activators phosphorylate the IκB protein, leading to rapid degradation of the IκB protein through the ubiquitin-proteasome pathway and NF-κB nuclear translocation [33]. RIP3 overexpression also activates the NF-κB signal pathway [34,35]. Published studies have shown the contribution of p38MAPK/NF-κB signaling to necroptosis in cardiomyocytes and other cells [36][37][38].…”

Section: Discussionmentioning

confidence: 99%

Polypeptide Globular Adiponectin Ameliorates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Inhibiting Both Apoptosis and Necroptosis

Zhu

Guo

et al. 2021

Journal of Immunology Research

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Adiponectin is a small peptide secreted and a key component of the endocrine system and immune system. Although globular adiponectin protects myocardial ischemia/reperfusion-induced cardiomyocyte injury, the protective mechanisms remain largely unresolved. Using a neonatal rat ventricular myocyte hypoxia/reoxygenation model, we investigated the role of its potential mechanisms of necroptosis in globular adiponectin-mediated protection in hypoxia/reoxygenation-induced cardiomyocyte injury as compared to apoptosis. We found that globular adiponectin treatment attenuated cardiomyocyte injury as indicated by increased cell viability and reduced lactate dehydrogenase release following hypoxia/reoxygenation. Immunofluorescence staining and Western blotting demonstrated that both necroptosis and apoptosis were triggered by hypoxia/reoxygenation and diminished by globular adiponectin. Necrostatin-1 (RIP1-specific inhibitor) and Z-VAD-FMK (pan-caspase inhibitor) only mimicked the inhibition of necroptosis and apoptosis, respectively, by globular adiponectin in hypoxia/reoxygenation-treated cardiomyocytes. Globular adiponectin attenuated reactive oxygen species production, oxidative damage, and p38MAPK and NF-κB signaling, all important for necroptosis and apoptosis. Collectively, our study suggests that globular adiponectin inhibits hypoxia/reoxygenation-induced necroptosis and apoptosis in cardiomyocytes probably by reducing oxidative stress and interrupting p38MAPK signaling.

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RIP3 overexpression sensitizes human breast cancer cells to parthenolide in vitro via intracellular ROS accumulation

Cited by 13 publications

References 32 publications

Resibufogenin suppresses colorectal cancer growth and metastasis through RIP3-mediated necroptosis

Resibufogenin suppresses colorectal cancer growth and metastasis through RIP3-mediated necroptosis

Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells

Polypeptide Globular Adiponectin Ameliorates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Inhibiting Both Apoptosis and Necroptosis

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