JWA regulates TRAIL-induced apoptosis via MARCH8-mediated DR4 ubiquitination in cisplatin-resistant gastric cancer cells

Wang, Q; Chen, Q; Zhu, Lei; Chen, M; Xu, Wenxia; Panday, Sapna; Wang, Z; Li, A; Røe, Oluf Dimitri; Chen, R; Wang, S; Zhang, R; Zhou, Jianwei

doi:10.1038/oncsis.2017.57

Cited by 28 publications

(23 citation statements)

References 46 publications

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“…Our results also showed that the regulation of STAT3 by JWA was not through the ERK/PI3K signaling pathway. Previous studies have shown that JWA can promote the ubiquitination and degradation of transcription factor Sp1 and death receptor 4 (DR4) by the proteasome 43 , 44 . Based on this, we speculate that JWA may promote the degradation of STAT3 through the ubiquitin–proteasome degradation pathway, and further investigation is required to test this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Astrocytic JWA deletion exacerbates dopaminergic neurodegeneration by decreasing glutamate transporters in mice

Wang

Zhao

et al. 2018

Cell Death Dis

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Astrocytic JWA exerts neuroprotective roles by alleviating oxidative stress and inhibiting inflammation. However, the molecular mechanisms of how astrocytic JWA is involved in dopaminergic neurodegeneration in Parkinson’s disease (PD) remain largely unknown. In this study, we found that astrocyte-specific JWA knockout mice (JWA CKO) exacerbated dopamine (DA) neuronal loss and motor dysfunction, and reduced the levels of DA and its metabolites in a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine/probenecid (MPTP/p)-induced PD model. Astrocytic JWA deficiency repressed expression of excitatory amino-acid transporter 2 (GLT-1) and glutamate uptake both in vivo and in vitro. Further, the regulation of GLT-1 expression was involved in JWA-triggered activation of the MAPK and PI3K signaling pathways. JWA-increased GLT-1 expression was abolished by inhibitors of MEK and PI3K. Silencing CREB also abrogated JWA-increased GLT-1 expression and glutamate uptake. Additionally, JWA deficiency activated glial fibrillary acidic protein (GFAP), and increased the expression of STAT3. Similarly to the MPTP model, paraquat (PQ) exposure produced PD-like phenotypes in JWA CKO mice. Taken together, our findings provide novel insights into astrocytic JWA function in the pathogenesis of neurotoxin mouse models of PD.

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Section: Discussionmentioning

confidence: 99%

Astrocytic JWA deletion exacerbates dopaminergic neurodegeneration by decreasing glutamate transporters in mice

Wang

Zhao

et al. 2018

Cell Death Dis

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“…Human GC SGC7901 cells and its cisplatin-resistant SGC7901/ DDP cells were kindly provided by Professor Jianwei Zhou (Nanjing Medical University) 33 . AGS cells and its cisplatinresistant AGS/DDP cells were obtained from Professor Chengchao Shou (Peking University Cancer Hospital & Institute) 27 .…”

Section: Cell Culture and Stable Transfectionmentioning

confidence: 99%

RNF138 confers cisplatin resistance in gastric cancer cells via activating Chk1 signaling pathway

Han

Liu

et al. 2018

Cancer Biology & Therapy

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Chemotherapy resistance represents a major issue associated with gastric cancer (GC) treatment, and arises through multiple mechanisms, including modulation of the cell-cycle check point. Several ubiquitin kinases, including RING finger protein 138 (RNF138), have been reported to mediate the G2/M phase arrest. In this study, we investigated the role of RNF138 in the development of cisplatin resistance of two GC cell lines. We show that RNF138 levels are higher in cisplatin-resistant cell lines, compared with cisplatin-sensitive cells, and RNF138 expression was elevated during drug withdrawal following the cisplatin treatment. Using gene overexpression and silencing, we analyzed the impact of altering RNF138 level on GC cell viability, apoptosis, and cell cycle phenotypes in two isogenic cisplatin-sensitive and resistant cell lines. We show that RNF138 overexpression increased GC cell viability, decreased apoptosis and delayed cell cycle progression in the cisplatin-sensitive GC cells. Conversely, RNF138 silencing produced opposite phenotypes in the cisplatin-resistant cells. Moreover, RNF138-dependent phosphorylation of Chk1 was seen in GC cells, indicating a novel connection between cisplatin-induced DNA damage and apoptosis. Collectively, these data suggest that RNF138 modulates the cisplatin resistance in the GC cells, thus serving as a potential drug target to challenge chemotherapy failure. In addition, RNF138 can also be used as a marker to monitor the development of cisplatin resistance in GC treatment. ARTICLE HISTORY

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“…Different ubiquitin ligases (e.g., MARCH8) have been shown to ubiquitinate DR4 at 273rd lysine and induce degradation [49]. CHIP (C terminus HSC70-interacting protein) induced the K6-linked polyubiquitylation of FADD and suppressed the formation of the DISC [13].…”

Section: Discussionmentioning

confidence: 99%

Natural Product Mediated Regulation of Death Receptors and Intracellular Machinery: Fresh from the Pipeline about TRAIL-Mediated Signaling and Natural TRAIL Sensitizers

Shahwar

Iqbal

Nisa³

et al. 2019

IJMS

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Rapidly developing resistance against different therapeutics is a major stumbling block in the standardization of therapy. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated signaling has emerged as one of the most highly and extensively studied signal transduction cascade that induces apoptosis in cancer cells. Rapidly emerging cutting-edge research has helped us to develop a better understanding of the signaling machinery involved in inducing apoptotic cell death. However, excitingly, cancer cells develop resistance against TRAIL-induced apoptosis through different modes. Loss of cell surface expression of TRAIL receptors and imbalance of stoichiometric ratios of pro- and anti-apoptotic proteins play instrumental roles in rewiring the machinery of cancer cells to develop resistance against TRAIL-based therapeutics. Natural products have shown excellent potential to restore apoptosis in TRAIL-resistant cancer cell lines and in mice xenografted with TRAIL-resistant cancer cells. Significantly refined information has previously been added and continues to enrich the existing pool of knowledge related to the natural-product-mediated upregulation of death receptors, rebalancing of pro- and anti-apoptotic proteins in different cancers. In this mini review, we will set spotlight on the most recently published high-impact research related to underlying mechanisms of TRAIL resistance and how these deregulations can be targeted by natural products to restore TRAIL-mediated apoptosis in different cancers.

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JWA regulates TRAIL-induced apoptosis via MARCH8-mediated DR4 ubiquitination in cisplatin-resistant gastric cancer cells

Cited by 28 publications

References 46 publications

Astrocytic JWA deletion exacerbates dopaminergic neurodegeneration by decreasing glutamate transporters in mice

Astrocytic JWA deletion exacerbates dopaminergic neurodegeneration by decreasing glutamate transporters in mice

RNF138 confers cisplatin resistance in gastric cancer cells via activating Chk1 signaling pathway

Natural Product Mediated Regulation of Death Receptors and Intracellular Machinery: Fresh from the Pipeline about TRAIL-Mediated Signaling and Natural TRAIL Sensitizers

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