Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.4
5.2
Journals
Cancers
Special Issues
Tumor-Associated Microenvironments and Inflammation
share announcement

Tumor-Associated Microenvironments and Inflammation

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 9330

Special Issue Editors

Prof. Dr. Ren Xu

E-Mail Website
Guest Editor
Markey Cancer Center, University of Kentucky, Lexington, KY 40536, USA
Interests: extracellular matrix; breast cancer metastasis; cancer-associated adipocyte; drug resistance
Prof. Dr. Bing Li

E-Mail Website
Guest Editor
Department of Microbiology and Immunology, School of Medicine, University of Louisville, Louisville, KY 40536, USA
Interests: breast cancer; obesity and immunoregulation; fatty acid binding proteins; cancer immunotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The tumor microenvironment (TME) is the complex non-cancerous cellular and non-cellular compartments presented in and around the tumor, including fibroblasts, immune cells, adipocytes, and cells that comprise the blood vessels. It has been shown that cancer cell plasticity and stemness are modulated by biochemical and biophysical sues derived from the TME, which in turn promotes cancer metastasis and therapeutic resistance. Cancer cells also produce a variety of growth factors and chemokines to modulate the function of fibroblasts, adipocytes, immune cells, and endothelial cells. The dynamic and reciprocal interaction between cancer cells and TME is crucial for cancer development and progression.

Targeting the TME has proven to be a promising strategy for cancer therapy. Angiogenesis inhibitors have been approved by the FDA for the treatment of solid tumors. Immunotherapy by targeting PD-1/PD-L1 and CTLA4 to enhance T cell function has revolutionized the field of oncology by prolonging the survival of cancer patients. Therefore, further elucidating the molecular and cellular biology of TME in cancer development and progression is critical for us to eventually eliminate cancer-related death. This Special Issue will highlight the current state of the art in the function and regulation of cancer-associated fibroblasts, adipocytes, immune cells, ECM remodeling, and prospects for improving TME-related therapies.

Prof. Dr. Ren Xu
Prof. Dr. Bing Li
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 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. 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
  • cancer-associated fibroblasts
  • adipocytes
  • immune cells
  • ECM remodeling
  • TME-related therapies

Published Papers (4 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

10 pages, 2870 KiB  
Article
Restoration of CD4+ T Cells during NAFLD without Modulation of the Hepatic Immunological Pattern Is Not Sufficient to Prevent HCC
by Madison Isbell, Faridoddin Mirshahi, Hussein F. Aqbi, Chunqing Guo, Mulugeta Saneshaw, Nicholas Koelsch, Michael O. Idowu, Dana Austin, Cohava Gelber, Xiang-Yang Wang, Arun J. Sanyal and Masoud H. Manjili
Cancers 2022, 14(22), 5502; https://doi.org/10.3390/cancers14225502 - 09 Nov 2022
Cited by 2 | Viewed by 1512
Abstract
Predominant inflammatory immunological patterns as well as the depletion of CD4+ T cells during nonalcoholic fatty liver disease (NAFLD) are reported to be associated with the progression of hepatocellular carcinoma (HCC). Here, we report that an LRP-1 agonistic peptide, SP16, when administered [...] Read more.
Predominant inflammatory immunological patterns as well as the depletion of CD4+ T cells during nonalcoholic fatty liver disease (NAFLD) are reported to be associated with the progression of hepatocellular carcinoma (HCC). Here, we report that an LRP-1 agonistic peptide, SP16, when administered during advanced NAFLD progression, restored the depleted CD4+ T cell population but did not significantly affect the inflammatory immunological pattern. This data suggests that restoration of CD4+ T cells without modulation of the hepatic immunological pattern is not sufficient to prevent HCC. However, SP16 administered early during NAFLD progression modulated the inflammatory profile. Future studies will determine if regulation of the inflammatory immune response by SP16 early in NAFLD progression will prevent HCC. Full article
(This article belongs to the Special Issue Tumor-Associated Microenvironments and Inflammation)
►▼ Show Figures

Figure 1

16 pages, 4696 KiB  
Article
CXCL8 Up-Regulated LSECtin through AKT Signal and Correlates with the Immune Microenvironment Modulation in Colon Cancer
by Shaojun Fang, Xianshuo Cheng, Tao Shen, Jian Dong, Yunfeng Li, Zhenhui Li, Linghan Tian, Yangwei Zhang, Xueyan Pan, Zhengfeng Yin and Zhibin Yang
Cancers 2022, 14(21), 5300; https://doi.org/10.3390/cancers14215300 - 28 Oct 2022
Cited by 4 | Viewed by 1580
Abstract
Background: The role of CXCL8 and LSECtin in colon cancer liver metastasis and immune checkpoint inhibitors (ICIs) treatment effect were widely recognized. However, the regulatory role of CXCL8 on LSECtin is still unclear. Methods: The expression of CXCL8 or LSECtin was analyzed by [...] Read more.
Background: The role of CXCL8 and LSECtin in colon cancer liver metastasis and immune checkpoint inhibitors (ICIs) treatment effect were widely recognized. However, the regulatory role of CXCL8 on LSECtin is still unclear. Methods: The expression of CXCL8 or LSECtin was analyzed by TCGA database, and verified by GES110225 and clinical samples. The relationship between the expression of CXCL8 or LSECtin and immune cells infiltration, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, Gene Ontology (GO) items, stromal score, Estimation of STromal and Immune cells in MAlignant Tumours (ESTIMAT) immune score, tumor mutation burden (TMB), mismatch repair gene and immune checkpoints expression were analyzed by Spearman. The effects of CXCL8 on LSECtin expression, proliferation, and invasion ability were clarified by recombinant CXCL8 or CXCL8 interfering RNA. Results: In colon cancer, the expression of CXCL8 was higher, but LSECtin was lower than that in normal mucosa. The expression of CXCL8 or LSECtin was significantly positively correlated with immune cells infiltration, stromal score, ESTIMATE immune score, TMB, and immune checkpoints expression. The expression of LSECtin was closely related to the cytokine-cytokine receptor interaction pathway and response of chemokine function, such as CXCL8/CXCR1/2 pathway. There was a significant positive correlation between the expression of CXCL8 and LSECtin in colon cancer. CXCL8 up-regulated LSECtin through AKT signal and promoted the proliferation and invasion ability of colon cancer. Conclusions: CXCL8 up-regulated LSECtin by activating AKT signal and correlated with the immune microenvironment modulation in colon cancer. Full article
(This article belongs to the Special Issue Tumor-Associated Microenvironments and Inflammation)
►▼ Show Figures

Figure 1

Review

Jump to: Research

15 pages, 1538 KiB  
Review
Role of FABP5 in T Cell Lipid Metabolism and Function in the Tumor Microenvironment
by Rong Jin, Jiaqing Hao, Jianyu Yu, Pingzhang Wang, Edward R. Sauter and Bing Li
Cancers 2023, 15(3), 657; https://doi.org/10.3390/cancers15030657 - 20 Jan 2023
Cited by 3 | Viewed by 2963
Abstract
To evade immune surveillance, tumors develop a hostile microenvironment that inhibits anti-tumor immunity. Recent immunotherapy breakthroughs that target the reinvigoration of tumor-infiltrating T lymphocytes (TIL) have led to unprecedented success in treating some cancers that are resistant to conventional therapy, suggesting that T [...] Read more.
To evade immune surveillance, tumors develop a hostile microenvironment that inhibits anti-tumor immunity. Recent immunotherapy breakthroughs that target the reinvigoration of tumor-infiltrating T lymphocytes (TIL) have led to unprecedented success in treating some cancers that are resistant to conventional therapy, suggesting that T cells play a pivotal role in anti-tumor immunity. In the hostile tumor microenvironment (TME), activated T cells are known to mainly rely on aerobic glycolysis to facilitate their proliferation and anti-tumor function. However, TILs usually exhibit an exhausted phenotype and impaired anti-tumor activity due to the limited availability of key nutrients (e.g., glucose) in the TME. Given that different T cell subsets have unique metabolic pathways which determine their effector function, this review introduces our current understanding of T cell development, activation signals and metabolic pathways. Moreover, emerging evidence suggests that fatty acid binding protein 5 (FABP5) expression in T cells regulates T cell lipid metabolism and function. We highlight how FABP5 regulates fatty acid uptake and oxidation, thus shaping the survival and function of different T cell subsets in the TME. Full article
(This article belongs to the Special Issue Tumor-Associated Microenvironments and Inflammation)
►▼ Show Figures

Figure 1

11 pages, 857 KiB  
Review
Obesity-Associated ECM Remodeling in Cancer Progression
by Junyan Li and Ren Xu
Cancers 2022, 14(22), 5684; https://doi.org/10.3390/cancers14225684 - 19 Nov 2022
Cited by 4 | Viewed by 2142
Abstract
Adipose tissue, an energy storage and endocrine organ, is emerging as an essential player for ECM remodeling. Fibrosis is one of the hallmarks of obese adipose tissue, featuring excessive ECM deposition and enhanced collagen alignment. A variety of ECM components and ECM-related enzymes [...] Read more.
Adipose tissue, an energy storage and endocrine organ, is emerging as an essential player for ECM remodeling. Fibrosis is one of the hallmarks of obese adipose tissue, featuring excessive ECM deposition and enhanced collagen alignment. A variety of ECM components and ECM-related enzymes are produced by adipocytes and myofibroblasts in obese adipose tissue. Data from lineage-tracing models and a single-cell analysis indicate that adipocytes can transform or de-differentiate into myofibroblast/fibroblast-like cells. This de-differentiation process has been observed under normal tissue development and pathological conditions such as cutaneous fibrosis, wound healing, and cancer development. Accumulated evidence has demonstrated that adipocyte de-differentiation and myofibroblasts/fibroblasts play crucial roles in obesity-associated ECM remodeling and cancer progression. In this review, we summarize the recent progress in obesity-related ECM remodeling, the mechanism underlying adipocyte de-differentiation, and the function of obesity-associated ECM remodeling in cancer progression. Full article
(This article belongs to the Special Issue Tumor-Associated Microenvironments and Inflammation)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop