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Biomedicines
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Roles of NF-κB in Cancer and Their Therapeutic Approaches 2019
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Roles of NF-κB in Cancer and Their Therapeutic Approaches 2019

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (8 April 2019) | Viewed by 18364

Special Issue Editor

Dr. Veronique Baud

E-Mail Website
Guest Editor
1. NF-kB, Differenciation and Cancer, University Paris Descartes, Sorbonne Paris Cité, 75014 Paris, France
2. Faculté de Pharmacie, 4 Avenue de l'Observatoire, 75006 Paris, France
Interests: interface between signal transduction and cancer with a focus on the alternative NF-kappaB signaling pathway, how it is regulated, and its contributions towards tumor development and resistance to conventional cancer therapies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Although mortality rates have declined in recent years, the majority of cancers are still difficult to treat and the medical need for better cancer treatments is evident. The current anticancer armamentarium includes many active agents that are applied across tumor types. However, most of these broadly-active anticancer drugs have a small therapeutic index and barely discriminate between malignant and normal cells. In recent years the focus has shifted to the development of rationally designed, molecularly-targeted therapy for the treatment of a specific cancer, therefore offering the promise of greater specificity coupled with reduced systemic toxicity. NF-κB transcription factor family as emerged as such a promising target for cancer therapy. This Special Issue will explore the routes from NF-κB basic research, cancer research and oncogenomics into the development of NF-κB-based cancer therapeutics and biomarkers.

We invite research and review papers in any area of the NF-κB field that are related, but not limited to, fundamental understanding of NF-κB signaling pathways, gene expression profiling, epigenetic regulation, diagnostic, prognostic and pharmacogenomic biomarkers, molecular targets driving the progression of human cancers, cancer drug development on these targets, clinical trial with new agents, and validation in animal models.

We hope that this Special Issue reflects the exciting era that we are living in with respect to the field of NF-κB and its applications in cancer research.

Dr. Veronique Baud
Guest Editor

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 short 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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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.

Keywords

  • NF-κB subunits
  • NF-κB signaling pathways
  • NF-κB related to:
  • solid tumors
  • hematological malignancies
  • oncogenomics
  • epigenetics
  • gene expression profiling
  • biomarkers
  • miRNA
  • ubiquitin-proteasome pathway
  • molecular targets
  • cancer targeted diagnosis
  • cancer targeted therapeutics
  • mechanism-based drug development
  • clinical trials
  • animal models

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Related Special Issue

Published Papers (3 papers)

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Research

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17 pages, 2777 KiB  
Article
Reporter Cell Assessment of TLR4-Induced NF-κB Responses to Cell-Free Hemoglobin and the Influence of Biliverdin
by Jill Sharma, Taylor Boyd, Claudia Alvarado, Edwin Gunn, Jaimie Adams, Traci Ness, Robert Dunwoody, John Lamb, Brittany House, James Knapp and Ronald Garner
Biomedicines 2019, 7(2), 41; https://doi.org/10.3390/biomedicines7020041 - 3 Jun 2019
Cited by 9 | Viewed by 5121
Abstract
Hemoglobin (Hb) released during red blood cell lysis can initiate TLR4-dependent signaling and trigger NF-κB activation in surrounding cells. Observations of chronic bleeding in various cancers leads us to hypothesize that Hb and Hb degradation products released from lysed RBC near cancer nests [...] Read more.
Hemoglobin (Hb) released during red blood cell lysis can initiate TLR4-dependent signaling and trigger NF-κB activation in surrounding cells. Observations of chronic bleeding in various cancers leads us to hypothesize that Hb and Hb degradation products released from lysed RBC near cancer nests might modulate local TLR4-positive cells. We addressed the hypothesis in vitro by measuring Hb- and biliverdin (Bv)-induced NF-κB signaling in an engineered human TLR4 reporter cell model (HEK-BlueTM hTLR4). Therein, TLR4 stimulation was assessed by measuring NF-κB-dependent secreted alkaline phosphatase (SEAP). hTLR4 reporter cells incubated with 8 ηM lipopolysaccharide (LPS) or 20-40 μM fungal mannoprotein (FM) produced significant amounts of SEAP. hTLR4 reporter cells also produced SEAP in response to human, but not porcine or bovine, Hb. HEK-Blue Null2TM reporter cells lacking TLR4 did not respond to LPS, FM, or Hb. Bv was non-stimulatory in reporter cells. When Bv was added to Hb-stimulated reporter cells, SEAP production was reduced by 95%, but when Bv was applied during LPS and FM stimulation, SEAP production was reduced by 33% and 27%, respectively. In conclusion, Hb initiated NF-κB signaling that was dependent upon TLR4 expression and that Bv can act as a TLR4 antagonist. Moreover, this study suggests that hemorrhage and extravascular hemolysis could provide competitive Hb and Bv signaling to nearby cells expressing TLR4, and that this process could modulate NF-κB signaling in TLR4-positive cancer cells and cancer-infiltrating leukocytes. Full article
(This article belongs to the Special Issue Roles of NF-κB in Cancer and Their Therapeutic Approaches 2019)
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13 pages, 1246 KiB  
Article
Controlling Nuclear NF-κB Dynamics by β-TrCP—Insights from a Computational Model
by Uwe Benary and Jana Wolf
Biomedicines 2019, 7(2), 40; https://doi.org/10.3390/biomedicines7020040 - 27 May 2019
Cited by 10 | Viewed by 4464
Abstract
The canonical nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway regulates central processes in mammalian cells and plays a fundamental role in the regulation of inflammation and immunity. Aberrant regulation of the activation of the transcription factor NF-κB is associated with [...] Read more.
The canonical nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway regulates central processes in mammalian cells and plays a fundamental role in the regulation of inflammation and immunity. Aberrant regulation of the activation of the transcription factor NF-κB is associated with severe diseases such as inflammatory bowel disease and arthritis. In the canonical pathway, the inhibitor IκB suppresses NF-κB’s transcriptional activity. NF-κB becomes active upon the degradation of IκB, a process that is, in turn, regulated by the β-transducin repeat-containing protein (β-TrCP). β-TrCP has therefore been proposed as a promising pharmacological target in the development of novel therapeutic approaches to control NF-κB’s activity in diseases. This study explores the extent to which β-TrCP affects the dynamics of nuclear NF-κB using a computational model of canonical NF-κB signaling. The analysis predicts that β-TrCP influences the steady-state concentration of nuclear NF-κB, as well as changes characteristic dynamic properties of nuclear NF-κB, such as fold-change and the duration of its response to pathway stimulation. The results suggest that the modulation of β-TrCP has a high potential to regulate the transcriptional activity of NF-κB. Full article
(This article belongs to the Special Issue Roles of NF-κB in Cancer and Their Therapeutic Approaches 2019)
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Review

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21 pages, 667 KiB  
Review
Evidence for the Involvement of the Master Transcription Factor NF-κB in Cancer Initiation and Progression
by Yu Rou Puar, Muthu K Shanmugam, Lu Fan, Frank Arfuso, Gautam Sethi and Vinay Tergaonkar
Biomedicines 2018, 6(3), 82; https://doi.org/10.3390/biomedicines6030082 - 27 Jul 2018
Cited by 168 | Viewed by 8003
Abstract
Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is responsible for the regulation of a large number of genes that are involved in important physiological processes, including survival, inflammation, and immune responses. At the same time, this transcription factor can control the expression [...] Read more.
Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is responsible for the regulation of a large number of genes that are involved in important physiological processes, including survival, inflammation, and immune responses. At the same time, this transcription factor can control the expression of a plethora of genes that promote tumor cell proliferation, survival, metastasis, inflammation, invasion, and angiogenesis. The aberrant activation of this transcription factor has been observed in several types of cancer and is known to contribute to aggressive tumor growth and resistance to therapeutic treatment. Although NF-κB has been identified to be a major contributor to cancer initiation and development, there is evidence revealing its role in tumor suppression. This review briefly highlights the major mechanisms of NF-κB activation, the role of NF-κB in tumor promotion and suppression, as well as a few important pharmacological strategies that have been developed to modulate NF-κB function. Full article
(This article belongs to the Special Issue Roles of NF-κB in Cancer and Their Therapeutic Approaches 2019)
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