Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.0
4.5
Journals
Cancers
Special Issues
Tumor Necrosis Factor (TNF)
share announcement

Tumor Necrosis Factor (TNF)

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 20240

Special Issue Editors

Dr. Lisa M. Sedger

E-Mail Website
Guest Editor
Faculty of Science, School of Life Sciences, University of Technology Sydney, Sydney, NSW 2007, Australia
Interests: intercellular vesicular; exosomes; cancer biology and treatments
Prof. Dr. Heinrich Korner

E-Mail Website
Guest Editor
Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS 7000, Australia
Interests: inflammation; inflammatory mediators; Tumor Necrosis Factor (TNF)

Special Issue Information

Dear Colleagues,

The impact of inflammation on tumors due to local bacterial infection has been known anecdotally since centuries and was recognized and implemented as experimental therapy by William Coley at the end of the 19th century. This early cancer “immunotherapy” proved unreliable but let to more work into a cytotoxic anti-tumoral factor which was finally isolated and termed tumor necrosis factor (TNF) in 1984. Over the last 35 years this initial discovery has sparked research that has resulted in the identification of large molecular families of ligands and receptors and their individual, vastly pleiotropic functions in cell physiology, cell death and the inflammatory and anti-tumoral response.

TNF, as well as a selected group of closely related, death-inducing members of the TNF super-family (TNFSF) act as pro- and anti-tumoral mediators, dependent on the environmental context. The range of activities of TNF in cancer includes (i) its capacity to trigger tumor cell apoptosis through its cognate death receptors, as cytotoxic factor that is expressed either as a soluble or transmembrane protein by cells involved in tumour surveillance, (ii) its role in intra-tumoral angiogenesis through receptor mediated activation of nuclear factor-kB (NF-kB), (iii) its influence in regulating cellular differentiation, especially macrophage (MØ) differentiation, and (iv) is mediation in T cell homeostasis by regulating T cell activation-induced cell death (AICD). Even after this long time new and surprising aspects of TNF functions are being revealed.  Thus, this collection of papers will attempt to communicate the new and emerging roles of TNF in the development and the spread of cancer.

We therefore invite papers that investigate cancer-specific TNF function with respect to (A) genomics and transcriptomics of tumorigenesis, (B) important aspects of TNF-Receptor mediated signalling pathways, (C) the influence in TNF and related TNF-SF in tumor surveillance and (D) AICD and T cell homeostasis, and any critical interactions with other cytokines involved in tumorigenesis and inflammatory mediators.

Dr. Lisa M. Sedger
Prof. Dr. Heinrich Korner
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (6 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

15 pages, 2406 KiB  
Article
Advantage of First-Line Therapeutic Drug Monitoring-Driven Use of Infliximab for Treating Acute Intestinal and Liver GVHD in Children: A Prospective, Single-Center Study
by Natalia Maximova, Daniela Nisticò, Guglielmo Riccio, Alessandra Maestro, Egidio Barbi, Barbara Faganel Kotnik, Annalisa Marcuzzi, Erika Rimondi and Antonello Di Paolo
Cancers 2023, 15(14), 3605; https://doi.org/10.3390/cancers15143605 - 13 Jul 2023
Cited by 2 | Viewed by 1403
Abstract
The high serum concentrations of TNF-α characterize acute graft-versus-host disease (aGVHD), for which infliximab treatment may be beneficial. In 28 pediatric patients, four doses of 10 mg/kg infliximab every seven days were administered after steroid failure (Standard Group, n = 14) or as [...] Read more.
The high serum concentrations of TNF-α characterize acute graft-versus-host disease (aGVHD), for which infliximab treatment may be beneficial. In 28 pediatric patients, four doses of 10 mg/kg infliximab every seven days were administered after steroid failure (Standard Group, n = 14) or as a first-line therapy (Early Group, n = 14). Population pharmacokinetic analyses and evaluation of serum cytokines were performed. After two months of treatment, complete response in gastrointestinal and liver aGVHD was achieved in 43% and 100% of patients in the Standard and Early groups, respectively. During follow-up, four patients in the Standard Group (but none in the Early Group) experienced an aGVHD recurrence. Viral infections occurred more frequently in the Standard Group after the fifth dose. Infliximab clearance did not differ between groups or according to treatment outcome for each organ involved in aGVHD, whereas serum levels of cytokines significantly differed. Therefore, present findings show that use of first-line, TDM-driven infliximab to treat aGVHD in children may result in better clinical outcomes and tolerability, with a different pattern of cytokines generated according to the moment of beginning of treatment. Full article
(This article belongs to the Special Issue Tumor Necrosis Factor (TNF))
►▼ Show Figures

Figure 1

19 pages, 4381 KiB  
Article
Tumour Necrosis Factor-Alpha (TNF-α)-Induced Metastatic Phenotype in Colorectal Cancer Epithelial Cells: Mechanistic Support for the Role of MicroRNA-21
by Aminah G. Alotaibi, Jia V. Li and Nigel J. Gooderham
Cancers 2023, 15(3), 627; https://doi.org/10.3390/cancers15030627 - 19 Jan 2023
Cited by 6 | Viewed by 3015
Abstract
Colorectal cancer is driven by genetic and epigenetic changes in cells to confer phenotypes that promote metastatic transformation and development. Tumour necrosis factor-alpha (TNF-α), a pro-inflammatory mediator, regulates cellular communication within the tumour microenvironment and is associated with the progression of the metastatic [...] Read more.
Colorectal cancer is driven by genetic and epigenetic changes in cells to confer phenotypes that promote metastatic transformation and development. Tumour necrosis factor-alpha (TNF-α), a pro-inflammatory mediator, regulates cellular communication within the tumour microenvironment and is associated with the progression of the metastatic phenotype. Oncogenic miR-21 has been shown to be overexpressed in most solid tumours, including colorectal cancer, and is known to target proteins involved in metastatic transformation. In this study, we investigated the relationship between TNF-α and miR-21 regulation in colorectal cancer epithelial cells (SW480 and HCT116). We observed that TNF-α, at concentrations reported to be present in serum and tumour tissue from colorectal cancer patients, upregulated miR-21 expression in both cell lines. TNF-α treatment also promoted cell migration, downregulation of the expression of E-cadherin, a marker of epithelial to mesenchymal transition, and anti-apoptotic BCL-2 (a validated target for miR-21). Knockdown of miR-21 had the opposite effect on each of these TNF-a induced phenotypic changes. Additionally, in the SW480 cell line, although TNF-α treatment selectively induced expression of a marker of metastatic progression VEGF-A, it failed to affect MMP2 expression or invasion activity. Our data indicate that exposing colorectal cancer epithelial cells to TNF-α, at concentrations occurring in the serum and tumour microenvironment of colorectal cancer patients, upregulated miR-21 expression and promoted the metastatic phenotype. Full article
(This article belongs to the Special Issue Tumor Necrosis Factor (TNF))
►▼ Show Figures

Figure 1

30 pages, 4463 KiB  
Article
Death Receptor 5 (TNFRSF10B) Is Upregulated and TRAIL Resistance Is Reversed in Hypoxia and Normoxia in Colorectal Cancer Cell Lines after Treatment with Skyrin, the Active Metabolite of Hypericum spp.
by Marián Babinčák, Rastislav Jendželovský, Ján Košuth, Martin Majerník, Jana Vargová, Kamil Mikulášek, Zbyněk Zdráhal and Peter Fedoročko
Cancers 2021, 13(7), 1646; https://doi.org/10.3390/cancers13071646 - 1 Apr 2021
Cited by 5 | Viewed by 3457
Abstract
Skyrin (SKR) is a plant bisanthraquinone secondary metabolite from the Hypericum genus with potential use in anticancer therapy. However, its effect and mechanism of action are still unknown. The negative effect of SKR on HCT 116 and HT-29 cancer cell lines in hypoxic [...] Read more.
Skyrin (SKR) is a plant bisanthraquinone secondary metabolite from the Hypericum genus with potential use in anticancer therapy. However, its effect and mechanism of action are still unknown. The negative effect of SKR on HCT 116 and HT-29 cancer cell lines in hypoxic and normoxic conditions was observed. HCT 116 cells were more responsive to SKR treatment as demonstrated by decreased metabolic activity, cellularity and accumulation of cells in the G1 phase. Moreover, an increasing number of apoptotic cells was observed after treatment with SKR. Based on the LC-MS comparative proteomic data from hypoxia and normoxia (data are available via ProteomeXchange with the identifier PXD019995), SKR significantly upregulated Death receptor 5 (DR5), which was confirmed by real-time qualitative PCR (RT-qPCR). Furthermore, multiple changes in the Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-activated cascade were observed. Moreover, the reversion of TRAIL resistance was observed in HCT 116, HT-29 and SW620 cell lines, even in hypoxia, which was linked to the upregulation of DR5. In conclusion, our results propose the use of SKR as a prospective anticancer drug, particularly as an adjuvant to TRAIL-targeting treatment to reverse TRAIL resistance in hypoxia. Full article
(This article belongs to the Special Issue Tumor Necrosis Factor (TNF))
►▼ Show Figures

Figure 1

20 pages, 4352 KiB  
Article
Loss of cIAP1 in Endothelial Cells Limits Metastatic Extravasation through Tumor-Derived Lymphotoxin Alpha
by Lazaros Vasilikos, Kay Hänggi, Lisanne M. Spilgies, Samanta Kisele, Stefanie Rufli and W. Wei-Lynn Wong
Cancers 2021, 13(4), 599; https://doi.org/10.3390/cancers13040599 - 3 Feb 2021
Cited by 3 | Viewed by 3258
Abstract
In this study, we determined whether Smac mimetics play a role in metastasis, specifically in circulation, tumor extravasation and growth in a metastatic site. Reports suggest inducing the degradation of IAPs through use of Smac mimetics, alters the ability of the tumor cell [...] Read more.
In this study, we determined whether Smac mimetics play a role in metastasis, specifically in circulation, tumor extravasation and growth in a metastatic site. Reports suggest inducing the degradation of IAPs through use of Smac mimetics, alters the ability of the tumor cell to metastasize. However, a role for the immune or stromal compartment in affecting the ability of tumor cells to metastasize upon loss of IAPs has not been defined. To address this open question, we utilized syngeneic tumor models in a late-stage model of metastasis. Loss of cIAP1 in the endothelial compartment, rather than depletion of cIAP2 or absence of cIAP1 in the hematopoietic compartment, caused reduction of tumor load in the lung. Our results underline the involvement of the endothelium in hindering tumor cell extravasation upon loss of cIAP1, in contrast to the immune compartment. Endothelial specific depletion of cIAP1 did not lead to cell death but resulted in an unresponsive endothelium barrier to permeability factors causing a decrease in tumor cell extravasation. Surprisingly, lymphotoxin alpha (LTA), and not TNF, secreted by the tumor cells, was critical for the extravasation. Using TCGA, we found high LTA mRNA expression correlated with decreased survival in kidney carcinoma and associated with advanced disease stage. Our data suggest that Smac mimetics, targeting cIAP1/2, reduce metastasis to the lung by inhibiting tumor cell extravasation. Full article
(This article belongs to the Special Issue Tumor Necrosis Factor (TNF))
►▼ Show Figures

Graphical abstract

Review

Jump to: Research

14 pages, 324 KiB  
Review
Tumor Necrosis Factor: What Is in a Name?
by Xinming Wang, Chunlan Yang, Heinrich Körner and Chaoliang Ge
Cancers 2022, 14(21), 5270; https://doi.org/10.3390/cancers14215270 - 27 Oct 2022
Cited by 6 | Viewed by 2981
Abstract
Tumor Necrosis Factor was one of the first cytokines described in the literature as a soluble mediator of cytotoxicity to tumors. Over the years, more extensive research that tried to employ Tumor Necrosis Factor in cancer treatments showed nevertheless that it mainly functioned [...] Read more.
Tumor Necrosis Factor was one of the first cytokines described in the literature as a soluble mediator of cytotoxicity to tumors. Over the years, more extensive research that tried to employ Tumor Necrosis Factor in cancer treatments showed nevertheless that it mainly functioned as a proinflammatory cytokine. However, this did not stop the search for the holy grail of cancer research: A cytokine that could act as a one-stop treatment for solid tumors and lymphomas. This review will summarize the long experimental history of Tumor Necrosis Factor that caused the initial observations of a tumor necrotizing cytokine that could serve as a potential cancer treatment and discuss the current state of research into this side of the activities of Tumor Necrosis Factor. Full article
(This article belongs to the Special Issue Tumor Necrosis Factor (TNF))
25 pages, 1757 KiB  
Review
Dual Role of TNF and LTα in Carcinogenesis as Implicated by Studies in Mice
by Ekaterina O. Gubernatorova, Almina I. Polinova, Mikhail M. Petropavlovskiy, Olga A. Namakanova, Alexandra D. Medvedovskaya, Ruslan V. Zvartsev, Georgij B. Telegin, Marina S. Drutskaya and Sergei A. Nedospasov
Cancers 2021, 13(8), 1775; https://doi.org/10.3390/cancers13081775 - 8 Apr 2021
Cited by 22 | Viewed by 4980
Abstract
Tumor necrosis factor (TNF) and lymphotoxin alpha (LTα) are two related cytokines from the TNF superfamily, yet they mediate their functions in soluble and membrane-bound forms via overlapping, as well as distinct, molecular pathways. Their genes are encoded within the major histocompatibility complex [...] Read more.
Tumor necrosis factor (TNF) and lymphotoxin alpha (LTα) are two related cytokines from the TNF superfamily, yet they mediate their functions in soluble and membrane-bound forms via overlapping, as well as distinct, molecular pathways. Their genes are encoded within the major histocompatibility complex class III cluster in close proximity to each other. TNF is involved in host defense, maintenance of lymphoid tissues, regulation of cell death and survival, and antiviral and antibacterial responses. LTα, known for some time as TNFβ, has pleiotropic functions including control of lymphoid tissue development and homeostasis cross talk between lymphocytes and their environment, as well as lymphoid tissue neogenesis with formation of lymphoid follicles outside the lymph nodes. Along with their homeostatic functions, deregulation of these two cytokines may be associated with initiation and progression of chronic inflammation, autoimmunity, and tumorigenesis. In this review, we summarize the current state of knowledge concerning TNF/LTα functions in tumor promotion and suppression, with the focus on the recently uncovered significance of host–microbiota interplay in cancer development that may explain some earlier controversial results. Full article
(This article belongs to the Special Issue Tumor Necrosis Factor (TNF))
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-6
Back to TopTop