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
Cancer, Immune-Control and Immunometabolism
share announcement

Cancer, Immune-Control and Immunometabolism

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

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 12706

Special Issue Editors

Prof. Dr. Lisardo Bosca

E-Mail Website
Guest Editor
Instituto de Investigaciones Biomédicas Alberto Sols (CSIC-UAM), Madrid 28029, Spain
Interests: cancer immunometabolism; cancer therapeutics; apoptosis; immunotherapy; cancer metabolism; colorectal cancer
Dr. Antonio Castrillo

E-Mail Website
Guest Editor
Instituto de Investigaciones Biomédicas "Alberto Sols", CSIC-UAM. Madrid, Spain and Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS)-Unidad de Biomedicina Unidad Asociada al CSIC, Universidad de Las Palmas de Gran Canaria, Las Palmas, Spain
Interests: transcriptional regulation; macrophage; nuclear receptors; inflammation; immunometabolism
Dr. Eduardo Lopez-Collazo

E-Mail Website
Guest Editor
Hospital la Paz Institute for Health Research (IdiPAZ), Madrid, Spain
Interests: innate immunity; sepsis; tumor immunology; cell fusion; immunotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent advances in our understanding of the interplay between cancer progression and metabolic responses in the microenvironment surrounding the tumor are providing a better comprehension of the protective mechanisms that fail to promote cancer cell suppression. A diversity of pathways contribute to alter the normal physiological immune control of malignant cells. These include the exacerbation of anaerobic glycolysis, as well as lesser-known mechanisms such as fatty acid synthesis, the provision of precursors to ensure cancer cell growth, and potential fusions between some malignant cells and cells of the immune system. Additional metabolic regulators in cancer include nuclear receptors, which may exert a direct action upon metabolic networks, including altered mitochondrial function and the release of factors that promote angiogenesis, tumor escape, and myeloid-cell tumoricidal actions. In addition to this, other metabolic aspects remain poorly studied, such as the role of glycogen in tumorigenesis and the metabolic regulation of the division cell cycle. We welcome works focusing on these metabolic adaptations between tumor cells and the environment, including the function of the immune cells.

Prof. Dr. Lisardo Bosca
Dr. Antonio Castrillo
Dr. Eduardo Lopez-Collazo
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

  • glycolysis
  • Warburg effect
  • lipogenesis
  • mitochondrial metabolism and cancer
  • amino acids metabolism in cancer
  • hypoxia regulators
  • nuclear receptors and cancer
  • immunotherapy
  • immune checkpoints
  • cell fusion and metabolism

Published Papers (3 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

11 pages, 9418 KiB  
Article
TET2 Inhibits PD-L1 Gene Expression in Breast Cancer Cells through Histone Deacetylation
by Yinghui Shen, Lu Liu, Mengyuan Wang, Bo Xu, Ruitu Lyu, Yujiang Geno Shi and Li Tan
Cancers 2021, 13(9), 2207; https://doi.org/10.3390/cancers13092207 - 04 May 2021
Cited by 19 | Viewed by 3179
Abstract
Activation of PD-1/PD-L1 checkpoint is a critical step for the immune evasion of malignant tumors including breast cancer. However, the epigenetic mechanism underlying the aberrant expression of PD-L1 in breast cancer cells remains poorly understood. To investigate the role of TET2 in the [...] Read more.
Activation of PD-1/PD-L1 checkpoint is a critical step for the immune evasion of malignant tumors including breast cancer. However, the epigenetic mechanism underlying the aberrant expression of PD-L1 in breast cancer cells remains poorly understood. To investigate the role of TET2 in the regulation of PD-L1 gene expression, quantitative reverse transcription PCR (RT-qPCR), Western blotting, chromatin immunoprecipitation (ChIP) assay and MeDIP/hMeDIP-qPCR were performed on MCF7 and MDA-MB-231 human breast cancer cells. Here, we reported that TET2 depletion upregulated PD-L1 gene expression in MCF7 cells. Conversely, ectopic expression of TET2 inhibited PD-L1 gene expression in MDA-MB-231 cells. Mechanistically, TET2 protein recruits histone deacetylases (HDACs) to PD-L1 gene promoter and orchestrates a repressive chromatin structure to suppress PD-L1 gene transcription, which is likely independent of DNA demethylation. Consistently, treatment with HDAC inhibitors upregulated PD-L1 gene expression in wild-type (WT) but not TET2 KO MCF7 cells. Furthermore, analysis of the CCLE and TCGA data showed a negative correlation between TET2 and PD-L1 expression in breast cancer. Taken together, our results identify a new epigenetic regulatory mechanism of PD-L1 gene transcription, linking the catalytic activity-independent role of TET2 to the anti-tumor immunity in breast cancer. Full article
(This article belongs to the Special Issue Cancer, Immune-Control and Immunometabolism)
►▼ Show Figures

Figure 1

Review

Jump to: Research

28 pages, 2426 KiB  
Review
Metabolic Hormones Modulate Macrophage Inflammatory Responses
by Matthew J. Batty, Gwladys Chabrier, Alanah Sheridan and Matthew C. Gage
Cancers 2021, 13(18), 4661; https://doi.org/10.3390/cancers13184661 - 17 Sep 2021
Cited by 9 | Viewed by 3784
Abstract
Macrophages are phagocytotic leukocytes that play an important role in the innate immune response and have established roles in metabolic diseases and cancer progression. Increased adiposity in obese individuals leads to dysregulation of many hormones including those whose functions are to coordinate metabolism. [...] Read more.
Macrophages are phagocytotic leukocytes that play an important role in the innate immune response and have established roles in metabolic diseases and cancer progression. Increased adiposity in obese individuals leads to dysregulation of many hormones including those whose functions are to coordinate metabolism. Recent evidence suggests additional roles of these metabolic hormones in modulating macrophage inflammatory responses. In this review, we highlight key metabolic hormones and summarise their influence on the inflammatory response of macrophages and consider how, in turn, these hormones may influence the development of different cancer types through the modulation of macrophage functions. Full article
(This article belongs to the Special Issue Cancer, Immune-Control and Immunometabolism)
►▼ Show Figures

Graphical abstract

22 pages, 1808 KiB  
Review
The Importance of Mitochondrial Pyruvate Carrier in Cancer Cell Metabolism and Tumorigenesis
by Ainhoa Ruiz-Iglesias and Santos Mañes
Cancers 2021, 13(7), 1488; https://doi.org/10.3390/cancers13071488 - 24 Mar 2021
Cited by 29 | Viewed by 5151
Abstract
Pyruvate is a key molecule in the metabolic fate of mammalian cells; it is the crossroads from where metabolism proceeds either oxidatively or ends with the production of lactic acid. Pyruvate metabolism is regulated by many enzymes that together control carbon flux. Mitochondrial [...] Read more.
Pyruvate is a key molecule in the metabolic fate of mammalian cells; it is the crossroads from where metabolism proceeds either oxidatively or ends with the production of lactic acid. Pyruvate metabolism is regulated by many enzymes that together control carbon flux. Mitochondrial pyruvate carrier (MPC) is responsible for importing pyruvate from the cytosol to the mitochondrial matrix, where it is oxidatively phosphorylated to produce adenosine triphosphate (ATP) and to generate intermediates used in multiple biosynthetic pathways. MPC activity has an important role in glucose homeostasis, and its alteration is associated with diabetes, heart failure, and neurodegeneration. In cancer, however, controversy surrounds MPC function. In some cancers, MPC upregulation appears to be associated with a poor prognosis. However, most transformed cells undergo a switch from oxidative to glycolytic metabolism, the so-called Warburg effect, which, amongst other possibilities, is induced by MPC malfunction or downregulation. Consequently, impaired MPC function might induce tumors with strong proliferative, migratory, and invasive capabilities. Moreover, glycolytic cancer cells secrete lactate, acidifying the microenvironment, which in turn induces angiogenesis, immunosuppression, and the expansion of stromal cell populations supporting tumor growth. This review examines the latest findings regarding the tumorigenic processes affected by MPC. Full article
(This article belongs to the Special Issue Cancer, Immune-Control and Immunometabolism)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop