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Advances in Cancer Metabolism and Tumour Microenvironment 3.0
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Advances in Cancer Metabolism and Tumour Microenvironment 3.0

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 (30 June 2023) | Viewed by 7342

Special Issue Editors

Dr. Michal Masarik

E-Mail Website1 Website2
Guest Editor
Department of Pathological Physiology, Department of Physiology, Faculty of Medicine, Masaryk University, Kamenice, 562500 Brno, Czech Republic
Interests: tumor biology; biochemistry and genetics
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Karel Smetana, Jr.

E-Mail Website1 Website2 Website3
Guest Editor
1st Faculty Medicine, Institute of Anatomy and BIOCEV, Charles University, Prague 2 and Vestec, Prague, Czech Republic
Interests: tumor microenvironment; cutaneous malignant melanoma; cancer-associated fibroblasts; squamous epithelium; stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

At the beginning of cancer research, attention was paid primarily to the characteristics of tumour cells themselves; however, the importance of the tumour microenvironment has been revealed gradually. The simple accumulation of mutations in cancer cells was shown to be insufficient for cancer progression and the formation of metastases. On the other hand, the key mechanisms of carcinogenesis were revealed in cell communication and metabolic interactions in the tumour microenvironment. These interactions are necessary for maintaining the energy and redox balance in cancer cells and encompass all stages of tumour development. How cancer cells acquire and use different metabolites and reprogramme their microenvironment to support tumour growth is an area of research that can have interesting therapeutic implications and a large impact on public health. Detecting metabolite level alterations in cancers may reveal an Achilles heel of cancer cells in the form of therapeutically targetable metabolic dependencies. Furthermore, because of metabolite alterations, epigenetic and gene expression changes can occur through altered DNA methylation or posttranslational protein modifications. These can lead to finding new applicable cancer biomarkers. Taken together, an altered cellular metabolism is undoubtedly a key hallmark of cancer, and an understanding of cancer metabolism will probably bring novel therapeutic approaches and new hope into cancer treatment.

Dr. Michal Masarik
Prof. Dr. Karel Smetana, Jr.
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. 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
  • metabolites
  • tumour microenvironment
  • cancer treatment
  • tumour growth
  • DNA methylation
  • epigenetic plasticity
  • hallmarks of cancer

Published Papers (4 papers)

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Research

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23 pages, 25022 KiB  
Article
MCL1 Inhibition Overcomes the Aggressiveness Features of Triple-Negative Breast Cancer MDA-MB-231 Cells
by Giovanni Pratelli, Daniela Carlisi, Diana Di Liberto, Antonietta Notaro, Michela Giuliano, Antonella D’Anneo, Marianna Lauricella, Sonia Emanuele, Giuseppe Calvaruso and Anna De Blasio
Int. J. Mol. Sci. 2023, 24(13), 11149; https://doi.org/10.3390/ijms241311149 - 6 Jul 2023
Viewed by 1464
Abstract
Triple-Negative Breast Cancer (TNBC) is a particularly aggressive subtype among breast cancers (BCs), characterized by anoikis resistance, high invasiveness, and metastatic potential as well as Epithelial–Mesenchymal Transition (EMT) and stemness features. In the last few years, our research focused on the function of [...] Read more.
Triple-Negative Breast Cancer (TNBC) is a particularly aggressive subtype among breast cancers (BCs), characterized by anoikis resistance, high invasiveness, and metastatic potential as well as Epithelial–Mesenchymal Transition (EMT) and stemness features. In the last few years, our research focused on the function of MCL1, an antiapoptotic protein frequently deregulated in TNBC. Here, we demonstrate that MCL1 inhibition by A-1210477, a specific BH3-mimetic, promotes anoikis/apoptosis in the MDA-MB-231 cell line, as shown via an increase in proapoptotic markers and caspase activation. Our evidence also shows A-1210477 effects on Focal Adhesions (FAs) impairing the integrin trim and survival signaling pathways, such as FAK, AKT, ERK, NF-κB, and GSK3β-inducing anoikis, thus suggesting a putative role of MCL1 in regulation of FA dynamics. Interestingly, in accordance with these results, we observed a reduction in migratory and invasiveness capabilities as confirmed by a decrease in metalloproteinases (MMPs) levels following A-1210477 treatment. Moreover, MCL1 inhibition promotes a reduction in EMT characteristics as demonstrated by the downregulation of Vimentin, MUC1, DNMT1, and a surprising re-expression of E-Cadherin, suggesting a possible mesenchymal-like phenotype reversion. In addition, we also observed the downregulation of stemness makers such as OCT3/4, SOX2, NANOG, as well as CD133, EpCAM, and CD49f. Our findings support the idea that MCL1 inhibition in MDA-MB-231 could be crucial to reduce anoikis resistance, aggressiveness, and metastatic potential and to minimize EMT and stemness features that distinguish TNBC. Full article
(This article belongs to the Special Issue Advances in Cancer Metabolism and Tumour Microenvironment 3.0)
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13 pages, 1472 KiB  
Article
Diverse Sphingolipid Profiles in Rectal and Colon Cancer
by Adam R. Markowski, Agnieszka U. Błachnio-Zabielska, Karolina Pogodzińska, Anna J. Markowska and Piotr Zabielski
Int. J. Mol. Sci. 2023, 24(13), 10867; https://doi.org/10.3390/ijms241310867 - 29 Jun 2023
Cited by 3 | Viewed by 1165
Abstract
Colorectal cancer is a heterogenous group of neoplasms showing a variety of clinical and pathological features depending on their anatomical location. Sphingolipids are involved in the formation and progression of cancers, and their changes are an important part of the abnormalities observed during [...] Read more.
Colorectal cancer is a heterogenous group of neoplasms showing a variety of clinical and pathological features depending on their anatomical location. Sphingolipids are involved in the formation and progression of cancers, and their changes are an important part of the abnormalities observed during carcinogenesis. Because the course of rectal and colonic cancer differs, the aim of the study was to assess whether the sphingolipid profile is also different in tumors of these two regions. Using a combination of ultra-high-performance liquid chromatography combined with triple quadrupole mass spectrometry, differences in the amounts of cellular sphingolipids were found in colorectal cancer. Sphingosine content was higher in rectal cancer than in adjacent healthy tissue, while the content of two ceramides (C18:0-Cer and C20:0-Cer) was lower. In colon cancer, a higher content of sphingosine, sphinganine, sphingosine-1-phosphate, and two ceramides (C14:0-Cer and C24:0-Cer) was found compared to healthy tissue, but there was no decrease in the amount of any of the assessed sphingolipids. In rectal cancer, the content of sphinganine and three ceramides (C16:0-Cer, C22:0-Cer, C24:0-Cer), as well as the entire pool of ceramides, was significantly lower compared to colon cancer. The S1P/Cer ratio in rectal cancer (S1P/C18:1-Cer, S1P/C20:0-Cer, S1P/C22:0-Cer, S1P/C24:1-Cer) and in colon cancer (S1P/C18:0-Cer, S1P/C18:1-Cer, S1P/C20:0-Cer) was higher than in adjacent healthy tissue and did not differ between the two sites (rectal cancer vs. colonic cancer). It seems that the development of colorectal cancer is accompanied by complex changes in the metabolism of sphingolipids, causing not only qualitative shifts in the ceramide pool of cancer tissue but also quantitative disturbances, depending on the location of the primary tumor. Full article
(This article belongs to the Special Issue Advances in Cancer Metabolism and Tumour Microenvironment 3.0)
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Review

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24 pages, 4831 KiB  
Review
The Involvement of Polyunsaturated Fatty Acids in Apoptosis Mechanisms and Their Implications in Cancer
by Mayra Montecillo-Aguado, Belen Tirado-Rodriguez and Sara Huerta-Yepez
Int. J. Mol. Sci. 2023, 24(14), 11691; https://doi.org/10.3390/ijms241411691 - 20 Jul 2023
Cited by 9 | Viewed by 2377
Abstract
Cancer is a significant global public health issue and, despite advancements in detection and treatment, the prognosis remains poor. Cancer is a complex disease characterized by various hallmarks, including dysregulation in apoptotic cell death pathways. Apoptosis is a programmed cell death process that [...] Read more.
Cancer is a significant global public health issue and, despite advancements in detection and treatment, the prognosis remains poor. Cancer is a complex disease characterized by various hallmarks, including dysregulation in apoptotic cell death pathways. Apoptosis is a programmed cell death process that efficiently eliminates damaged cells. Several studies have indicated the involvement of polyunsaturated fatty acids (PUFAs) in apoptosis, including omega-3 PUFAs such as alpha-linolenic acid, docosahexaenoic acid, and eicosapentaenoic acid. However, the role of omega-6 PUFAs, such as linoleic acid, gamma-linolenic acid, and arachidonic acid, in apoptosis is controversial, with some studies supporting their activation of apoptosis and others suggesting inhibition. These PUFAs are essential fatty acids, and Western populations today have a high consumption rate of omega-6 to omega-3 PUFAs. This review focuses on presenting the diverse molecular mechanisms evidence in both in vitro and in vivo models, to help clarify the controversial involvement of omega-3 and omega-6 PUFAs in apoptosis mechanisms in cancer. Full article
(This article belongs to the Special Issue Advances in Cancer Metabolism and Tumour Microenvironment 3.0)
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18 pages, 1771 KiB  
Review
Potential Chemopreventive Role of Pterostilbene in Its Modulation of the Apoptosis Pathway
by Omchit Surien, Siti Fathiah Masre, Dayang Fredalina Basri and Ahmad Rohi Ghazali
Int. J. Mol. Sci. 2023, 24(11), 9707; https://doi.org/10.3390/ijms24119707 - 3 Jun 2023
Cited by 4 | Viewed by 1939
Abstract
Cancer incidence keeps increasing every year around the world and is one of the leading causes of death worldwide. Cancer has imposed a major burden on the human population, including the deterioration of physical and mental health as well as economic or financial [...] Read more.
Cancer incidence keeps increasing every year around the world and is one of the leading causes of death worldwide. Cancer has imposed a major burden on the human population, including the deterioration of physical and mental health as well as economic or financial loss among cancer patients. Conventional cancer treatments including chemotherapy, surgery, and radiotherapy have improved the mortality rate. However, conventional treatments have many challenges; for example, drug resistance, side effects, and cancer recurrence. Chemoprevention is one of the promising interventions to reduce the burden of cancer together with cancer treatments and early detection. Pterostilbene is a natural chemopreventive compound with various pharmacological properties such as anti-oxidant, anti-proliferative, and anti-inflammatory properties. Moreover, pterostilbene, due to its potential chemopreventive effect on inducing apoptosis in eliminating the mutated cells or preventing the progression of premalignant cells to cancerous cells, should be explored as a chemopreventive agent. Hence, in the review, we discuss the role of pterostilbene as a chemopreventive agent against various types of cancer via its modulation of the apoptosis pathway at the molecular levels. Full article
(This article belongs to the Special Issue Advances in Cancer Metabolism and Tumour Microenvironment 3.0)
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