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Cancers
Special Issues
IFN-Gamma Signaling in Cancer
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IFN-Gamma Signaling in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Immunology and Immunotherapy".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 1771

Special Issue Editor

Prof. Dr. Ivana Vancurova

E-Mail Website
Guest Editor
Department of Biological Sciences, St. John's University, New York, NY, USA
Interests: cancer immunology; transcriptional regulation; cytokines; PD-L1; NFkB
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are thrilled to announce a Special Issue titled "IFN-Gamma Signaling in Cancer". This Special Issue focuses on the intricate signaling pathways and molecular mechanisms through which IFNγ influences cancer development and progression. Since early studies revealed IFNγ’s strong anti-tumor effects, which include its activation of immune cells, cell cycle arrest, and increased cancer cell apoptosis, IFNγ has been used in cancer treatment. In addition, IFNγ expression is induced by radiation and immune checkpoint blockades used in anti-cancer therapies. However, mounting evidence indicates that IFNγ also has important tumor promoting functions that include its ability to induce expression of the immune checkpoint ligand PD-L1 and T cell exhaustion, cancer cell proliferation, and tumor growth.

This Special Issue aims to explore the multifaceted effects of IFNγ on cancer biology. It encompasses understanding how IFNγ influences tumor cell growth and survival, immune cell activation and function, PD-L1 expression and immune escape, and the intricate crosstalk between tumor cells and the tumor microenvironment. A better understanding of the mechanisms and biological significance of the anti-tumor and tumor-promoting IFNγ signaling in cancer cells will lead to the development of novel strategies aimed at increasing IFNγ’s effectiveness in cancer treatment and in anti-cancer therapies associated with increased IFNγ expression, such as radiation and immune checkpoint blockades.

We invite researchers, academicians, and practitioners to contribute original research articles, reviews, and communications that advance our understanding of the role of IFNγ signaling in cancer.

Prof. Dr. Ivana Vancurova
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 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.

Keywords

  • IFN-gamma signaling
  • tumor immunology
  • immunotherapy
  • immune checkpoint blockade
  • immune evasion
  • PD-L1
  • tumor microenvironment

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Published Papers (1 paper)

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23 pages, 2156 KiB  
Review
IFNγ-Induced Bcl3, PD-L1 and IL-8 Signaling in Ovarian Cancer: Mechanisms and Clinical Significance
by Suprataptha U. Reddy, Fatema Zohra Sadia, Ales Vancura and Ivana Vancurova
Cancers 2024, 16(15), 2676; https://doi.org/10.3390/cancers16152676 - 27 Jul 2024
Viewed by 1463
Abstract
IFNγ, a pleiotropic cytokine produced not only by activated lymphocytes but also in response to cancer immunotherapies, has both antitumor and tumor-promoting functions. In ovarian cancer (OC) cells, the tumor-promoting functions of IFNγ are mediated by IFNγ-induced expression of Bcl3, PD-L1 and IL-8/CXCL8, [...] Read more.
IFNγ, a pleiotropic cytokine produced not only by activated lymphocytes but also in response to cancer immunotherapies, has both antitumor and tumor-promoting functions. In ovarian cancer (OC) cells, the tumor-promoting functions of IFNγ are mediated by IFNγ-induced expression of Bcl3, PD-L1 and IL-8/CXCL8, which have long been known to have critical cellular functions as a proto-oncogene, an immune checkpoint ligand and a chemoattractant, respectively. However, overwhelming evidence has demonstrated that these three genes have tumor-promoting roles far beyond their originally identified functions. These tumor-promoting mechanisms include increased cancer cell proliferation, invasion, angiogenesis, metastasis, resistance to chemotherapy and immune escape. Recent studies have shown that IFNγ-induced Bcl3, PD-L1 and IL-8 expression is regulated by the same JAK1/STAT1 signaling pathway: IFNγ induces the expression of Bcl3, which then promotes the expression of PD-L1 and IL-8 in OC cells, resulting in their increased proliferation and migration. In this review, we summarize the recent findings on how IFNγ affects the tumor microenvironment and promotes tumor progression, with a special focus on ovarian cancer and on Bcl3, PD-L1 and IL-8/CXCL8 signaling. We also discuss promising novel combinatorial strategies in clinical trials targeting Bcl3, PD-L1 and IL-8 to increase the effectiveness of cancer immunotherapies. Full article
(This article belongs to the Special Issue IFN-Gamma Signaling in Cancer)
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