Cancer Metabolic Landscapes and Interactions

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

Deadline for manuscript submissions: closed (20 January 2024) | Viewed by 1536

Special Issue Editor


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Guest Editor
Health School of the Polytechnic Institute of Guarda, Guarda, Portugal
Interests: cancer; metabolism; mitochondria; microenvironment crosstalk

Special Issue Information

Dear Colleagues,

The groundbreaking finding of Otto Warburg in the 1920s preceded the beginning of oncometabolism, now a recognized very fast-moving field of research. Metabolism’s complexity and interconnection with cell networks is as much an appealing as a challenging topic of research. Cellular metabolic adaptations, now a recognized hallmark of cancer, possess clear implications in many cellular processes extending from proliferation to survival. Mitochondria sits at the center of tumors’ energetics, virtually influencing all contributing factors in oncogenic processes. A comprehensive insight into underlining the cancer metabolic plasticity repertoire as a bidirectional crosstalk with genetics, epigenetics, or the microenvironment is necessary. This Special Issue of Cancers aims to clarify and collate the latest research on how the cancer cell metabolism changes and affects the molecular processes of tumorigenesis. Original research articles and review contributions are encouraged from areas that may include, but are not limited to, metabolism, mitochondria, metastasis, microenvironment, stem cells, and coding and noncoding RNA.

I look forward to receiving your contributions.    

Dr. Ricardo Marques
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.

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

  • mitochondria
  • metabolomics
  • microenvironment
  • RNA modifications
  • metastasis
  • cancer stem cells

Published Papers (1 paper)

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Research

11 pages, 1620 KiB  
Article
Deletion of PGAM5 Downregulates FABP1 and Attenuates Long-Chain Fatty Acid Uptake in Hepatocellular Carcinoma
by Ganesan Muthusamy, Chin-Chi Liu and Andrea N. Johnston
Cancers 2023, 15(19), 4796; https://doi.org/10.3390/cancers15194796 - 29 Sep 2023
Viewed by 1289
Abstract
Phosphoglycerate mutase 5 (PGAM5) is a Ser/His/Thr phosphatase responsible for regulating mitochondrial homeostasis. Overexpression of PGAM5 is correlated with a poor prognosis in hepatocellular carcinoma, colon cancer, and melanoma. In hepatocellular carcinoma, silencing of PGAM5 reduces growth, which has been attributed to decreased [...] Read more.
Phosphoglycerate mutase 5 (PGAM5) is a Ser/His/Thr phosphatase responsible for regulating mitochondrial homeostasis. Overexpression of PGAM5 is correlated with a poor prognosis in hepatocellular carcinoma, colon cancer, and melanoma. In hepatocellular carcinoma, silencing of PGAM5 reduces growth, which has been attributed to decreased mitophagy and enhanced apoptosis. Yet in colon cancer, PGAM5’s pro-tumor survival effect is correlated to lipid metabolism. We sought to identify whether deletion of PGAM5 modulated lipid droplet accrual in hepatocellular carcinoma. HepG2 and Huh7 PGAM5 knockout cell lines generated using CRISPR/Cas9 technology were used to measure cell growth, cellular ATP, and long-chain fatty acid uptake. Expression of hepatocellular fatty acid transporters, cluster of differentiation 36 (CD36), solute carrier family 27 member 2 (SLC27A2), solute carrier family 27 member 5 (SLC27A5), and fatty acid binding protein 1 (FABP1) was measured by quantitative PCR and Western blot. We found that deletion of PGAM5 attenuates hepatocellular carcinoma cell growth and ATP production. Further, PGAM5 knockout ameliorates palmitate-induced steatosis and reduces expression of FABP1 in HepG2 and Huh7 cell lines. PGAM5’s role in hepatocellular carcinoma includes regulation of fatty acid metabolism, which may be related to expression of the fatty acid transporter, FABP1. Full article
(This article belongs to the Special Issue Cancer Metabolic Landscapes and Interactions)
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