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Cancers
Special Issues
Immune System Pathways in Inflammatory Tumor Microenvironment and Carcinogenesis
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Immune System Pathways in Inflammatory Tumor Microenvironment and Carcinogenesis

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

Deadline for manuscript submissions: closed (29 December 2023) | Viewed by 8141

Special Issue Editors

Prof. Dr. Jörg Kleeff

E-Mail Website
Guest Editor
Department of Visceral, Vascular and Endocrine Surgery, University Hospital Halle (Saale), Ernst-Grube-Str. 40, 06120 Halle, Germany
Interests: pancreatic cancer; clinical research; surgery; translational research; microenvironment
Special Issues, Collections and Topics in MDPI journals
Dr. Yoshiaki Sunami

E-Mail Website
Guest Editor
Department of Visceral, Vascular and Endocrine Surgery, Martin-Luther-University Halle-Wittenberg, University Medical Center Halle, 06120 Halle, Germany
Interests: pancreatic and hepatocellular carcinogenesis; stromal reaction; cancer-associated fibroblasts; inflammation; NASH; tumor metabolism especially lipid metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

While inflammatory processes are indispensable to fighting acute infection, inflammatory mediators in a chronic situation are associated with the development of a stromal microenvironment and the induction of carcinogenesis. The tumor microenvironment includes various immune cell populations, cancer-associated fibroblasts (CAFs), and endothelial cells, resulting in an abundant collection of growth factors, inflammatory cytokines, and chemokines, which regulate paracrine signaling activities between the different cellular compartments. This Special Issue aims to describe the recent findings and advances in understanding paracrine regulation and immune system pathways in the inflammatory tumor microenvironment and molecular mechanism of carcinogenesis, as well as immunotherapeutic strategies.

Prof. Dr. Jörg Kleeff
Dr. Yoshiaki Sunami
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.

Keywords

  • tumor microenvironment
  • cytokines and chemokines
  • paracrine regulation
  • chronic inflammation
  • carcinogenesis
  • inflammation and immune system pathways
  • cancer immunotherapy

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Published Papers (3 papers)

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Research

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19 pages, 4081 KiB  
Article
GPR4 Knockout Attenuates Intestinal Inflammation and Forestalls the Development of Colitis-Associated Colorectal Cancer in Murine Models
by Mona A. Marie, Edward J. Sanderlin, Alexander P. Hoffman, Kylie D. Cashwell, Swati Satturwar, Heng Hong, Ying Sun and Li V. Yang
Cancers 2023, 15(20), 4974; https://doi.org/10.3390/cancers15204974 - 13 Oct 2023
Cited by 5 | Viewed by 2669
Abstract
GPR4 is a proton-sensing G protein-coupled receptor highly expressed in vascular endothelial cells and has been shown to potentiate intestinal inflammation in murine colitis models. Herein, we evaluated the proinflammatory role of GPR4 in the development of colitis-associated colorectal cancer (CAC) using the [...] Read more.
GPR4 is a proton-sensing G protein-coupled receptor highly expressed in vascular endothelial cells and has been shown to potentiate intestinal inflammation in murine colitis models. Herein, we evaluated the proinflammatory role of GPR4 in the development of colitis-associated colorectal cancer (CAC) using the dextran sulfate sodium (DSS) and azoxymethane (AOM) mouse models in wild-type and GPR4 knockout mice. We found that GPR4 contributed to chronic intestinal inflammation and heightened DSS/AOM-induced intestinal tumor burden. Tumor blood vessel density was markedly reduced in mice deficient in GPR4, which correlated with increased tumor necrosis and reduced tumor cell proliferation. These data demonstrate that GPR4 ablation alleviates intestinal inflammation and reduces tumor angiogenesis, development, and progression in the AOM/DSS mouse model. Full article
(This article belongs to the Special Issue Immune System Pathways in Inflammatory Tumor Microenvironment and Carcinogenesis)
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19 pages, 3826 KiB  
Article
Exploring the Tumor-Suppressing Potential of PSCA in Pancreatic Ductal Adenocarcinoma
by Kexin Li, Qingji Huo, Kazumasa Minami, Keisuke Tamari, Kazuhiko Ogawa, Sungsoo Na, Melissa L. Fishel, Bai-Yan Li and Hiroki Yokota
Cancers 2023, 15(20), 4917; https://doi.org/10.3390/cancers15204917 - 10 Oct 2023
Cited by 1 | Viewed by 2257
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with low survival rates. We explored an innovative therapeutic approach by leveraging prognostic oncogenic markers. Instead of inhibiting these marker genes, we harnessed their tumor-modifying potential in the extracellular domain. Surprisingly, many of the proteins [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with low survival rates. We explored an innovative therapeutic approach by leveraging prognostic oncogenic markers. Instead of inhibiting these marker genes, we harnessed their tumor-modifying potential in the extracellular domain. Surprisingly, many of the proteins highly expressed in PDAC, which is linked to poor survival, exhibited tumor-suppressing qualities in the extracellular environment. For instance, prostate stem cell antigens (PSCA), associated with reduced survival, acted as tumor suppressors when introduced extracellularly. We performed in vitro assays to assess the proliferation and migration and evaluated the tumor-modifying capacity of extracellular factors from peripheral blood mononuclear cells (PBMCs) in PDAC tissues. Molecular docking analysis, immunoprecipitation, Western blotting, and RNA interference were employed to study the regulatory mechanism. Extracellular PSCA recombinant protein notably curtailed the viability, motility, and transwell invasion of PDAC cells. Its anti-PDAC effects were partially mediated by Mesothelin (MSLN), another highly expressed tumor-associated antigen in PDAC. The anti-tumor effects of extracellular PSCA complemented those of chemotherapeutic agents like Irinotecan, 5-Fluorouracil, and Oxaliplatin. PSCA expression increased in a conditioned medium derived from PBMCs and T lymphocytes. This study unveils the paradoxical anti-PDAC potential of PSCA, hinting at the dual roles of oncoproteins like PSCA in PDAC suppression. Full article
(This article belongs to the Special Issue Immune System Pathways in Inflammatory Tumor Microenvironment and Carcinogenesis)
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Review

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23 pages, 1081 KiB  
Review
Paracrine Regulation and Immune System Pathways in the Inflammatory Tumor Microenvironment of Lung Cancer: Insights into Oncogenesis and Immunotherapeutic Strategies
by Firas Batrash, Adnan Shaik, Rayaan Rauf, Mahmoud Kutmah and Jun Zhang
Cancers 2024, 16(6), 1113; https://doi.org/10.3390/cancers16061113 - 10 Mar 2024
Cited by 1 | Viewed by 2287
Abstract
The intricate interplay between inflammatory processes and the tumor microenvironment (TME) in lung cancer has garnered increasing attention due to its implications for both oncogenesis and therapeutic strategies. In this review, we explore recent advances in understanding the paracrine regulation and immune system [...] Read more.
The intricate interplay between inflammatory processes and the tumor microenvironment (TME) in lung cancer has garnered increasing attention due to its implications for both oncogenesis and therapeutic strategies. In this review, we explore recent advances in understanding the paracrine regulation and immune system pathways within the inflammatory TME of lung cancer. We delve into the molecular mechanisms underpinning oncogenesis, highlighting the role of immune cell populations, cancer-associated fibroblasts, and endothelial cells, as well as their interactions through immune system pathways regulated in a paracrine pattern. Additionally, we discuss emerging immunotherapeutic strategies with a specific focus on the potential of leveraging the inflammatory TME through these pathways to enhance treatment efficacy in lung cancer. Full article
(This article belongs to the Special Issue Immune System Pathways in Inflammatory Tumor Microenvironment and Carcinogenesis)
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