Membrane-bound TNF mediates microtubule-targeting chemotherapeutics-induced cancer cytolysis via juxtacrine inter-cancer-cell death signaling

Zhang, Jing; Ye, Yu; Zhou, Shenao; He, Xueyan; Wu, Chenlu; Hu, Hong Yu; Qin, Jie; Wei, Gang; Wang, Huayi; Liu, Suling; Sun, Liming

doi:10.1038/s41418-019-0441-3

Cited by 12 publications

(6 citation statements)

References 68 publications

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“…c-JUN is known as an important transcription factor involved in many carcinogenic processes, especially in cell cycle progression, 48 anti-apoptotic activity, 49 and cell proliferation, 50 and it serves as a downstream effector of the PI3K / AKT signal. 51 , 52 It was reported to be involved in many miRNAs’ regulation as a transcription factor, such as miR-374a 53 , 54 and miR-3188.…”

Section: Discussionmentioning

confidence: 99%

miR-4721, Induced by EBV-miR-BART22, Targets GSK3β to Enhance the Tumorigenic Capacity of NPC through the WNT/β-catenin Pathway

Tang

Chen

et al. 2020

Molecular Therapy - Nucleic Acids

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Nasopharyngeal carcinoma (NPC) is prevalent in East and Southeast Asia. In a previous study, Epstein-Barr virus (EBV)-miR-BART22 induces tumor metastasis and stemness and is significantly involved in NPC progression. In the present study, we observed that miR-4721 is induced by EBV-miR-BART22 through phosphatidylinositol 3-kinase (PI3K)/AKT/c-JUN/Sp1 signaling to promote its transcription. In a subsequent study, we observed that miR-4721 serves as a potential oncogenic factor promoting NPC cell cycle progression and cell proliferation in vitro and in vivo . Mechanism analysis indicated that miR-4721 directly targetes GSK3β and reduces its expression, which therefore elevates β-catenin intra-nuclear aggregation and activates its downstream cell cycle factors, including CCND1 and c-MYC. In clinical samples, miR-4721 and GSK3β are respectively observed to be upregulated and downregulated in NPC progression. Elevated expression of miR-4721 is positively associated with clinical progression and poor prognosis. Our study first demonstrated that miR-4721 as an oncogene is induced by EBV-miR-BART22 via modulating PI3K/AKT/c-JUN/Sp1 signaling to target GSK3β, which thus activates the WNT/β-catenin-stimulated cell cycle signal and enhances the tumorigenic capacity in NPC. miR-4721 may be a potential biomarker or therapeutic target in NPC treatment in the future.

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Section: Discussionmentioning

confidence: 99%

miR-4721, Induced by EBV-miR-BART22, Targets GSK3β to Enhance the Tumorigenic Capacity of NPC through the WNT/β-catenin Pathway

Tang

Chen

et al. 2020

Molecular Therapy - Nucleic Acids

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“…In turn, IL1b has a plethora of pro-cancerogenic effects [ 191 ]; however, it can also induce the anti-cancerogenic Th1 polarisation [ 192 ] and is regulated by the p73/caspase1/inflammasome axis [ 150 , 193 ]. p73-mediated caspase-1 expression is induced by TNFa that also induces a pro-cancerogenic program in SSC [ 63 ] but apoptosis in endothelial cells, respectively [ 165 , 194 , 195 , 196 ]. The TAp73-induced expression of BGN inhibits the TGFb pro-oncogenic signalling [ 122 ].…”

Section: Figurementioning

confidence: 99%

Dual Role of p73 in Cancer Microenvironment and DNA Damage Response

Rozenberg

Zvereva

Dalina

et al. 2021

Cells

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Understanding the mechanisms that regulate cancer progression is pivotal for the development of new therapies. Although p53 is mutated in half of human cancers, its family member p73 is not. At the same time, isoforms of p73 are often overexpressed in cancers and p73 can overtake many p53 functions to kill abnormal cells. According to the latest studies, while p73 represses epithelial–mesenchymal transition and metastasis, it can also promote tumour growth by modulating crosstalk between cancer and immune cells in the tumor microenvironment, M2 macrophage polarisation, Th2 T-cell differentiation, and angiogenesis. Thus, p73 likely plays a dual role as a tumor suppressor by regulating apoptosis in response to genotoxic stress or as an oncoprotein by promoting the immunosuppressive environment and immune cell differentiation.

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“…TNF directly induces apoptosis and necrosis in tumor cells ( Adjuto-Saccone et al, 2021 ). It elevates the expression of death receptors on tumor cell surfaces, binding to them to activate downstream apoptotic pathways ( Zhang et al, 2020 ). Furthermore, TNF enhances the cytotoxic activity of immune effector cells, such as macrophages and NK cells, against tumor cells ( Müller and Kontermann, 2010 ).…”

Section: Discussionmentioning

confidence: 99%

Unveiling the landscape of cytokine research in glioma immunotherapy: a scientometrics analysis

Zhang,

Chen,

Jiang

et al. 2024

Front. Pharmacol.

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Background: Cytokines modulate the glioma tumor microenvironment, influencing occurrence, progression, and treatment response. Strategic cytokine application may improve glioma immunotherapy outcomes. Gliomas remain refractory to standard therapeutic modalities, but immunotherapy shows promise given the integral immunomodulatory roles of cytokines. However, systematic evaluation of cytokine glioma immunotherapy research is absent. Bibliometric mapping of the research landscape, recognition of impactful contributions, and elucidation of evolutive trajectories and hot topics has yet to occur, potentially guiding future efforts. Here, we analyzed the structure, evolution, trends, and hotspots of the cytokine glioma immunotherapy research field, subsequently focusing on avenues for future investigation.Methods: This investigation conducted comprehensive bibliometric analyses on a corpus of 1529 English-language publications, from 1 January 2000, to 4 October 2023, extracted from the Web of Science database. The study employed tools including Microsoft Excel, Origin, VOSviewer, CiteSpace, and the Bibliometrix R package, to systematically assess trends in publication, contributions from various countries, institutions, authors, and journals, as well as to examine literature co-citation and keyword distributions within the domain of cytokines for glioma immunotherapy. The application of these methodologies facilitated a detailed exploration of the hotspots, the underlying knowledge structure, and the developments in the field of cytokines for glioma immunotherapy.Results: This bibliometric analysis revealed an exponential growth in annual publications, with the United States, China, and Germany as top contributors. Reviews constituted 17% and research articles 83% of total publications. Analysis of keywords like “interleukin-13,” “TGF-beta,” and “dendritic cells” indicated progression from foundational cytokine therapies to sophisticated understanding of the tumor microenvironment and immune dynamics. Key research avenues encompassed the tumor microenvironment, epidermal growth factor receptor, clinical trials, and interleukin pathways. This comprehensive quantitative mapping of the glioma immunotherapy cytokine literature provides valuable insights to advance future research and therapeutic development.Conclusion: This study has identified remaining knowledge gaps regarding the role of cytokines in glioma immunotherapy. Future research will likely focus on the tumor microenvironment, cancer vaccines, epidermal growth factor receptor, and interleukin-13 receptor alpha 2. Glioma immunotherapy development will continue through investigations into resistance mechanisms, microglia and macrophage biology, and interactions within the complex tumor microenvironment.

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Membrane-bound TNF mediates microtubule-targeting chemotherapeutics-induced cancer cytolysis via juxtacrine inter-cancer-cell death signaling

Cited by 12 publications

References 68 publications

miR-4721, Induced by EBV-miR-BART22, Targets GSK3β to Enhance the Tumorigenic Capacity of NPC through the WNT/β-catenin Pathway

miR-4721, Induced by EBV-miR-BART22, Targets GSK3β to Enhance the Tumorigenic Capacity of NPC through the WNT/β-catenin Pathway

Dual Role of p73 in Cancer Microenvironment and DNA Damage Response

Unveiling the landscape of cytokine research in glioma immunotherapy: a scientometrics analysis

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