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Cancer Metabolism—Metabolites Regulation of Oncogenic Signaling and Epigenetics 2.0

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 (31 January 2021) | Viewed by 6001

Special Issue Editor

Special Issue Information

Dear Colleagues,

This Special Issue focuses on mechanisms and regulations in the altered metabolic pathways in cancer cells.

Cancer has been considered a disorder of proliferation, but recent evidence suggests that cancer is also a metabolic disease. The fact that growing tumors rewire their metabolic programs was first recognized almost a century ago. Now, links between oncogenic pathways and cancer-cell metabolism have been established. Cancer cells alter their metabolism to meet their energetic and anabolic demands and to survive in hostile environments.

The cancer metabolome is extremely flexible, creating challenges for drug discovery, as cancers can often bypass the effects of a small molecule by shifting pathways. A better understanding of cancer-specific metabolic processes may revolutionize cancer treatment.

Metabolic remodeling in cancer creates metabolites that control the signaling and epigenetic pathways that drive tumors. Understanding the interaction between metabolism and signaling/epigenetic pathways could reveal new vulnerabilities of cancer.

We welcome submissions, including original manuscripts and reviews, on this important topic.

Dr. Jun-ichi Hanai
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 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.

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Keywords

  • impact of oncogenic signaling on metabolism
  • alterations in metabolite-driven gene regulation and signaling pathways
  • metabolic wiring
  • metabolic control of the epigenome
  • metabolic heterogeneity and cancer progression
  • targeting metabolic liabilities
  • targeting stroma metabolism
  • cancer metabolism influenced by systemic metabolic status
  • immunometabolism
  • redox metabolism
  • the influence of metabolism on metastasis and progression
  • Warburg in non-cancer diseases,inflammation
  • metabolism-based imaging
  • preclinical and clinical studies of metabolism-related cancer therapies

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Published Papers (1 paper)

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Review

33 pages, 3690 KiB  
Review
Reprogramming of Mesothelial-Mesenchymal Transition in Chronic Peritoneal Diseases by Estrogen Receptor Modulation and TGF-β1 Inhibition
by Robert B. Wilson, Rami Archid and Marc A. Reymond
Int. J. Mol. Sci. 2020, 21(11), 4158; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21114158 - 10 Jun 2020
Cited by 20 | Viewed by 5534
Abstract
In chronic peritoneal diseases, mesothelial-mesenchymal transition is determined by cues from the extracellular environment rather than just the cellular genome. The transformation of peritoneal mesothelial cells and other host cells into myofibroblasts is mediated by cell membrane receptors, Transforming Growth Factor β1 (TGF-β1), [...] Read more.
In chronic peritoneal diseases, mesothelial-mesenchymal transition is determined by cues from the extracellular environment rather than just the cellular genome. The transformation of peritoneal mesothelial cells and other host cells into myofibroblasts is mediated by cell membrane receptors, Transforming Growth Factor β1 (TGF-β1), Src and Hypoxia-inducible factor (HIF). This article provides a narrative review of the reprogramming of mesothelial mesenchymal transition in chronic peritoneal diseases, drawing on the similarities in pathophysiology between encapsulating peritoneal sclerosis and peritoneal metastasis, with a particular focus on TGF-β1 signaling and estrogen receptor modulators. Estrogen receptors act at the cell membrane/cytosol as tyrosine kinases that can phosphorylate Src, in a similar way to other receptor tyrosine kinases; or can activate the estrogen response element via nuclear translocation. Tamoxifen can modulate estrogen membrane receptors, and has been shown to be a potent inhibitor of mesothelial-mesenchymal transition (MMT), peritoneal mesothelial cell migration, stromal fibrosis, and neoangiogenesis in the treatment of encapsulating peritoneal sclerosis, with a known side effect and safety profile. The ability of tamoxifen to inhibit the transduction pathways of TGF-β1 and HIF and achieve a quiescent peritoneal stroma makes it a potential candidate for use in cancer treatments. This is relevant to tumors that spread to the peritoneum, particularly those with mesenchymal phenotypes, such as colorectal CMS4 and MSS/EMT gastric cancers, and pancreatic cancer with its desmoplastic stroma. Morphological changes observed during mesothelial mesenchymal transition can be treated with estrogen receptor modulation and TGF-β1 inhibition, which may enable the regression of encapsulating peritoneal sclerosis and peritoneal metastasis. Full article
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