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Molecular Insights into Cancer Metabolism, Metastasis, and Immune Evasion

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (30 November 2024) | Viewed by 3281

Special Issue Editor

Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA
Interests: metastasis; molecular pathway; cancer models; metabolism; tumor microenvironment; drug screening and development
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metastatic disease is responsible for approximately 90% of cancer deaths. In order for metastasis to be successful, cancer cells must evade detection and destruction by the immune system. This evasion is facilitated by factors secreted by the primary tumor that shape both the intratumoral microenvironment and the systemic immune landscape. While some components of the immune system contribute to antitumor immunity, others are involved in tumor progression. There is increasing evidence that tumors continuously interact with the immune system by altering their metabolic pathways to adapt to different microenvironments and therapeutic interventions. Therefore, targeting cancer metabolic heterogeneity represents an innovative therapeutic strategy with the potential to prevent metastasis and the immune escape of cancer cells.

This Special Issue aims to advance our understanding of the mechanistic basis of cancer metabolism, metastasis, and immune evasion. We seek to bridge three major topics—cancer metabolism, metastasis, and immune evasion—with a particular focus on molecular determinants and regulations. Our goal is to formulate novel mechanism-driven counter-strategies and therapeutic combinations to facilitate clinical translation. Original research articles and comprehensive reviews are welcome for submission to this Special Issue. Articles are expected to cover, but are not limited to, the following topics:

  1. Tumor–immune cell crosstalk in metastasis formation.
  2. Mechanistic insights into how primary tumors hijack tumor–immune interactions to enhance their metastatic potential.
  3. The molecular mechanisms involved in the intricate interactions within cancer metabolism.
  4. The metabolic patterns and heterogeneity in tumor developmental stages, ranging from initiation to metastasis.
  5. Potential approaches to manipulating the tumor–immune interactome for therapeutic benefits.

Dr. Yong Teng
Guest Editor

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cancer metabolism
  • metastasis
  • immune evasion
  • tumor–immune interactions
  • combination therapy

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Published Papers (2 papers)

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Research

16 pages, 5192 KiB  
Article
The Immunosuppressive Receptor CD32b Regulation of Macrophage Polarization and Its Implications in Tumor Progression
by Hong-Jing Chuang, Ying-Yin Chen, Yi-Da Chung, Evelyn Huang, Cadence Yoshang Huang, Jrhau Lung, Chung-Yu Chen and Hui-Fen Liao
Int. J. Mol. Sci. 2024, 25(17), 9737; https://doi.org/10.3390/ijms25179737 - 9 Sep 2024
Cited by 1 | Viewed by 1711
Abstract
Macrophages, pivotal components of the immune system, orchestrate host defense mechanisms in humans and mammals. Their polarization into classically activated macrophages (CAMs or M1) and alternatively activated macrophages (AAMs or M2) dictates distinct functional roles in immunity and tissue homeostasis. While the negative [...] Read more.
Macrophages, pivotal components of the immune system, orchestrate host defense mechanisms in humans and mammals. Their polarization into classically activated macrophages (CAMs or M1) and alternatively activated macrophages (AAMs or M2) dictates distinct functional roles in immunity and tissue homeostasis. While the negative regulatory role of CD32b within the FC gamma receptor (FCγR) family is recognized across various immune cell types, its influence on macrophage polarization remains elusive. This study aimed to elucidate the regulatory role of CD32b in macrophage polarization and discern the differential expression markers between the M1 and M2 phenotypes following CD32b siRNA transfection. The results revealed a decrease in the CD32b levels in lipopolysaccharide (LPS)-treated M1 and an increase in interleukin-4 (IL-4)-treated M2 macrophages, as observed in macrophage Raw264.7 cells. Furthermore, CD32b siRNA transfection significantly downregulated the M2 markers (IL-10, VEGF, Arg-1, and STAT6), while upregulating the M1 markers (IL-6, NF-κB, NOS2, and STAT1) in the Raw264.7 cells. Similar findings were recapitulated in macrophage-rich adherent cells isolated from mouse spleens. Additionally, the cytopathological analysis of pleural effusions and ascitic fluids from patients with cancer revealed a positive correlation between advanced tumor stages, metastasis, and elevated CD32b levels. In conclusion, this study highlights the regulatory influence of CD32b in suppressing M1 expression and promoting M2 polarization. Moreover, heightened M2 activation and CD32b levels appear to correlate with tumor progression. A targeted CD32b blockade may serve as a novel therapeutic strategy to inhibit M2 macrophage polarization and is promising for anti-tumor intervention. Full article
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15 pages, 5152 KiB  
Article
Serum TLR2 and TLR9 in Prostate Cancer Patients in Relation to EBV Status
by Dominika Sikora, Jacek Kiś, Ewa Stępień, Bartłomiej Drop and Małgorzata Polz-Dacewicz
Int. J. Mol. Sci. 2024, 25(16), 9053; https://doi.org/10.3390/ijms25169053 - 21 Aug 2024
Cited by 1 | Viewed by 1072
Abstract
The relationship between Toll-like receptors (TLRs) and prostate cancer (PCa) is complex due to the presence of the Epstein–Barr virus (EBV) infection, which has been identified as a predisposing factor for some cancers, including PCa. The present study aims to investigate these complex [...] Read more.
The relationship between Toll-like receptors (TLRs) and prostate cancer (PCa) is complex due to the presence of the Epstein–Barr virus (EBV) infection, which has been identified as a predisposing factor for some cancers, including PCa. The present study aims to investigate these complex links by examining the levels of selected TLRs and the potential impact of EBV infection on PCa. Therefore, we examined the serum of patients with PCa. The study compared EBV(+) patients to risk groups, the Gleason score (GS), and the T-trait. Additionally, the correlation between TLR and antibody levels was examined. The results indicated that higher levels of TLR-2 and TLR-9 were observed in more advanced PCa. The findings of this study may contribute to a deeper understanding of the role of viral infections in PCa and provide information on future strategies for the diagnosis, prevention, and treatment of these malignancies. Full article
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