Submit to Special Issue Submit Abstract to Special Issue Review for Cancers Propose a Special Issue

Journal Menu

Journal Browser

► Journal Browser

Special Issue "Lipids and Small Metabolites in Cancer"

Special Issue Editors
Special Issue Information
Keywords
Published Papers

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

Deadline for manuscript submissions: 30 March 2024 | Viewed by 4015

Share This Special Issue

Special Issue Editors

Dr. Zsolt Balogi

E-Mail Website
Guest Editor

Institute of Biochemistry and Medical Chemistry, Medical School, University of Pecs, Szigeti str. 12, 7624 Pecs, Hungary
Interests: cancer; trafficking; lipid

Dr. Laszlo Vigh

E-Mail Website
Guest Editor

Biological Research Center of the Hungarian Academy of Sciences, H-6726 Szeged, Hungary
Interests: heat shock proteins; stress sensing- and signaling; lipidomics; membrane fluidity and membrane homeostasis

Special Issue Information

Dear Colleagues,

Small molecule metabolites, such as amino acids, fatty acids, lipids, and numerous components of biochemical pathways, have emerged as a characteristic feature of tumor development. A wealth of omics data identified changes in the metabolome and the lipidome as a new hallmark of tumorigenesis. Understanding around pathological changes in the complex metabolome and lipidome has drastically improved. Cluster and pathway analyses of large datasets are inevitable bioinformatic tools to decode specific molecular patterns and their functions involved in the pathogenesis of tumors. The functional rewiring of disease-affected molecular cohorts can fuel complex multimodal therapeutic solutions with improved capacity to overcome resistance mechanisms.

This Special Issue, titled “Lipids and small metabolites in cancer”, welcomes all aspects of metabolome- and lipidome-related cancer research and review articles for a comprehensive view of this special topic based on omics screens, bioinformatics, targeted analyses, in vitro and in vivo experimental, or clinical results.

Dr. Zsolt Balogi
Dr. Laszlo Vigh
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

lipid
small metabolites
cancer
metabolome- and lipidome-related
amino acids
fatty acids
numerous components of biochemical pathways

Published Papers (3 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

20 pages, 4239 KiB

Open AccessArticle

The Combined Inhibition of Autophagy and Diacylglycerol Acyltransferase-Mediated Lipid Droplet Biogenesis Induces Cancer Cell Death during Acute Amino Acid Starvation

and

Cancers 2023, 15(19), 4857; https://doi.org/10.3390/cancers15194857 - 05 Oct 2023

Viewed by 666

Abstract

Lipid droplets (LDs) are dynamic organelles involved in the management of fatty acid trafficking and metabolism. Recent studies suggest that autophagy and LDs serve complementary roles in the protection against nutrient stress, but the autophagy–LD interplay in cancer cells is not well understood. Here, we examined the relationship between autophagy and LDs in starving HeLa cervical cancer- and MDA-MB-231 breast cancer cells. We found that acute amino acid depletion induces autophagy and promotes diacylglycerol acyltransferase 1 (DGAT1)-mediated LD accumulation in HeLa cells. Inhibition of autophagy via late-stage autophagy inhibitors, or by knocking down autophagy-related 5 (ATG5), reduced LD accumulation in amino acid-starved cancer cells, suggesting that autophagy contributes to LD biogenesis. On the contrary, knockdown of adipose triglyceride lipase (ATGL) increased LD accumulation, suggesting that LD breakdown is mediated by lipolysis under these conditions. Concurrent inhibition of autophagy by silencing ATG5 and of LD biogenesis using DGAT inhibitors was effective in killing starving HeLa cells, whereas cell survival was not compromised by suppression of ATGL-mediated lipolysis. Autophagy-dependent LD biogenesis was also observed in the aggressive triple-negative MDA-MB-231 breast cancer cells deprived of amino acids, but these cells were not sensitized to starvation by the combined inhibition of LD biogenesis and autophagy. These findings reveal that while targeting autophagy-driven and DGAT-mediated LD biogenesis reduces the resilience of HeLa cervical cancer cells to amino acid deprivation, this strategy may not be successful in other cancer cell types. Full article

(This article belongs to the Special Issue Lipids and Small Metabolites in Cancer)

► Show Figures

Figure 1

13 pages, 1789 KiB

Open AccessEditor’s ChoiceArticle

Plasma Metabolomics Predicts Chemotherapy Response in Advanced Pancreatic Cancer

Veronica Placencio-Hickok

and

Cancers 2023, 15(11), 3020; https://doi.org/10.3390/cancers15113020 - 01 Jun 2023

Cited by 1 | Viewed by 1102

Abstract

Pancreatic cancer (PC) is one of the deadliest cancers. Developing biomarkers for chemotherapeutic response prediction is crucial for improving the dismal prognosis of advanced-PC patients (pts). To evaluate the potential of plasma metabolites as predictors of the response to chemotherapy for PC patients, we analyzed plasma metabolites using high-performance liquid chromatography–mass spectrometry from 31 cachectic, advanced-PC subjects enrolled into the PANCAX-1 (NCT02400398) prospective trial to receive a jejunal tube peptide-based diet for 12 weeks and who were planned for palliative chemotherapy. Overall, there were statistically significant differences in the levels of intermediates of multiple metabolic pathways in pts with a partial response (PR)/stable disease (SD) vs. progressive disease (PD) to chemotherapy. When stratified by the chemotherapy regimen, PD after 5-fluorouracil-based chemotherapy (e.g., FOLFIRINOX) was associated with decreased levels of amino acids (AAs). For gemcitabine-based chemotherapy (e.g., gemcitabine/nab-paclitaxel), PD was associated with increased levels of intermediates of glycolysis, the TCA cycle, nucleoside synthesis, and bile acid metabolism. These results demonstrate the feasibility of plasma metabolomics in a prospective cohort of advanced-PC patients for assessing the effect of enteral feeding as their primary source of nutrition. Metabolic signatures unique to FOLFIRINOX or gemcitabine/nab-paclitaxel may be predictive of a patient’s response and warrant further study. Full article

(This article belongs to the Special Issue Lipids and Small Metabolites in Cancer)

► Show Figures

Figure 1

Review

Jump to: Research

37 pages, 4133 KiB

Open AccessReview

Biosynthesis and Significance of Fatty Acids, Glycerophospholipids, and Triacylglycerol in the Processes of Glioblastoma Tumorigenesis

and

Irena Baranowska-Bosiacka

Cancers 2023, 15(7), 2183; https://doi.org/10.3390/cancers15072183 - 06 Apr 2023

Cited by 2 | Viewed by 1685

Abstract

One area of glioblastoma research is the metabolism of tumor cells and detecting differences between tumor and healthy brain tissue metabolism. Here, we review differences in fatty acid metabolism, with a particular focus on the biosynthesis of saturated fatty acids (SFA), monounsaturated fatty acids (MUFA), and polyunsaturated fatty acids (PUFA) by fatty acid synthase (FASN), elongases, and desaturases. We also describe the significance of individual fatty acids in glioblastoma tumorigenesis, as well as the importance of glycerophospholipid and triacylglycerol synthesis in this process. Specifically, we show the significance and function of various isoforms of glycerol-3-phosphate acyltransferases (GPAT), 1-acylglycerol-3-phosphate O-acyltransferases (AGPAT), lipins, as well as enzymes involved in the synthesis of phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylserine (PS), phosphatidylinositol (PI), and cardiolipin (CL). This review also highlights the involvement of diacylglycerol O-acyltransferase (DGAT) in triacylglycerol biosynthesis. Due to significant gaps in knowledge, the GEPIA database was utilized to demonstrate the significance of individual enzymes in glioblastoma tumorigenesis. Finally, we also describe the significance of lipid droplets in glioblastoma and the impact of fatty acid synthesis, particularly docosahexaenoic acid (DHA), on cell membrane fluidity and signal transduction from the epidermal growth factor receptor (EGFR). Full article

(This article belongs to the Special Issue Lipids and Small Metabolites in Cancer)

► Show Figures

Journal Menu

Journal Browser

Special Issue "Lipids and Small Metabolites in Cancer"

Share This Special Issue

Special Issue Editors

Special Issue Information

Keywords

Published Papers (3 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI