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Biomedicines
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Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives...
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Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 6266

Special Issue Editor

Dr. Francesco Ciccarese

E-Mail Website
Guest Editor
Istituto Oncologico Veneto IOV-IRCCS, via Gattamelata 64, 35128 Padova, Italy
Interests: reactive oxygen species; redox homeostasis; electron transport chain; mitochondria; cancer metabolism; apoptosis; anticancer strategies; autophagy; drug development; viruses; angiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic rewiring is a common feature of cancer cells which promotes tumorigenesis by sustaining uncontrolled proliferation, survival in an adverse microenvironment, invasion, metastasis and resistance to anticancer therapies. Cancer cells tightly control catabolic and anabolic reactions through a plethora of processes, including oncogenic activation, loss of tumor suppressors, genetic alterations in metabolic genes, epigenetic regulation and modulation by both microRNAs and long non-coding RNAs. Moreover, there is evidence that oncogenic viruses also impinge on these pathways to induce malignant transformation. Evasion of cell death is the leading cause of therapeutic failure. In this regard, cancer metabolism impacts on the response of cancer cells to treatment by activating pro-survival processes, including autophagy, or favoring immune escape by modulating the tumor microenvironment. The pivotal role of metabolic reprogramming in the resistance of cancer cells to different types of cell death, including apoptosis and ferroptosis, provides the rationale for anticancer strategies aimed at rewiring cancer cell metabolism. Such approaches have the potential to enhance the sensitivity of cancer cells to conventional and targeted therapies. This Special Issue of Biomedicines aims at dissecting the multifaceted connections between cancer metabolism and cell death pathways, with a focus on the pharmacological modulation of tumor metabolism as an anticancer strategy.

Dr. Francesco Ciccarese
Guest Editor

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Keywords

  • cancer metabolism
  • cell death
  • oncogenic activation
  • miRNAs and lncRNAs
  • oncogenic viruses
  • sensitization to anticancer therapies

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Related Special Issue

Published Papers (3 papers)

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Research

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17 pages, 2965 KiB  
Article
Preliminary Metabolomics Study Suggests Favorable Metabolic Changes in the Plasma of Breast Cancer Patients after Surgery and Adjuvant Treatment
by Andrea Jiménez-Franco, Juan Manuel Jiménez-Aguilar, Marta Canela-Capdevila, Raquel García-Pablo, Helena Castañé, Cristian Martínez-Navidad, Pablo Araguas, Bárbara Malavé, Rocío Benavides-Villarreal, Johana C. Acosta, Alina Iuliana Onoiu, Navita Somaiah, Jordi Camps, Jorge Joven and Meritxell Arenas
Biomedicines 2024, 12(10), 2196; https://doi.org/10.3390/biomedicines12102196 - 26 Sep 2024
Cited by 1 | Viewed by 1496
Abstract
Background/Objectives: The management of early breast cancer (BC) includes surgery, followed by adjuvant radiotherapy, chemotherapy, hormone therapy, or immunotherapy. However, the influence of these interventions in metabolic reprogramming remains unknown. This study explored alterations in the plasma metabolome of BC patients following [...] Read more.
Background/Objectives: The management of early breast cancer (BC) includes surgery, followed by adjuvant radiotherapy, chemotherapy, hormone therapy, or immunotherapy. However, the influence of these interventions in metabolic reprogramming remains unknown. This study explored alterations in the plasma metabolome of BC patients following distinct treatments to deepen our understanding of BC pathophysiology, outcomes, and the identification of potential biomarkers. Methods: We included 52 women diagnosed with BC and candidates for surgery as primary oncological treatment. Blood samples were collected at diagnosis, two weeks post-surgery, and one month post-radiotherapy. Plasma samples from 49 healthy women served as controls. Targeted metabolomics assessed 74 metabolites spanning carbohydrates, amino acids, lipids, nucleotide pathways, energy metabolism, and xenobiotic biodegradation. Results: Before treatment, the BC patients exhibited notable changes in carbohydrate, nucleotide, lipid, and amino acid metabolism. We noticed a gradual restoration of specific metabolite levels (hypoxanthine, 3-phosphoglyceric acid, xylonic acid, and maltose) throughout different treatments, suggesting a normalization of the nucleotide and carbohydrate metabolic pathways. Moreover, we observed increased dodecanoic acid concentrations, a metabolite associated with cancer protection. These variations distinguished patients from controls with high specificity and sensitivity. Conclusions: Our preliminary study suggests that oncological treatments modify the metabolism of patients towards a favorable profile with a decrease in the pathways that favor cell proliferation and an increase in the levels of anticancer molecules. These findings emphasize the pivotal role of metabolomics in recognizing the biological pathways influenced by each cancer treatment and the resulting metabolic consequences. Furthermore, it aids in identifying potential biomarkers for disease onset and progression. Full article
(This article belongs to the Special Issue Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives 2nd Edition)
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17 pages, 2337 KiB  
Article
Modulation of Epithelial–Mesenchymal Transition Is a Possible Underlying Mechanism for Inducing Chemoresistance in MIA PaCa-2 Cells against Gemcitabine and Paclitaxel
by Hajime Nakamura, Megumi Watanabe, Kohichi Takada, Tatsuya Sato, Fumihito Hikage, Araya Umetsu, Joji Muramatsu, Masato Furuhashi and Hiroshi Ohguro
Biomedicines 2024, 12(5), 1011; https://doi.org/10.3390/biomedicines12051011 - 3 May 2024
Cited by 3 | Viewed by 2417
Abstract
To elucidate the currently unknown molecular mechanisms responsible for the similarity and difference during the acquirement of resistance against gemcitabine (GEM) and paclitaxel (PTX) in patients with pancreatic carcinoma, we examined two-dimensional (2D) and three-dimensional (3D) cultures of parent MIA PaCa-2 cells (MIA [...] Read more.
To elucidate the currently unknown molecular mechanisms responsible for the similarity and difference during the acquirement of resistance against gemcitabine (GEM) and paclitaxel (PTX) in patients with pancreatic carcinoma, we examined two-dimensional (2D) and three-dimensional (3D) cultures of parent MIA PaCa-2 cells (MIA PaCa-2-PA) and their GEM resistance cell line (MIA PaCa-2-GR) and PTX resistance (MIA PaCa-2-PR). Using these cells, we examined 3D spheroid configurations and cellular metabolism, including mitochondrial and glycolytic functions, with a Seahorse bio-analyzer and RNA sequencing analysis. Compared to the MIA PaCa-2-PA, (1) the formation of the 3D spheroids of MIA PaCa-2-GR or -PR was much slower, and (2) their mitochondrial and glycolytic functions were greatly modulated in MIA PaCa-2-GR or -PR, and such metabolic changes were also different between their 2D and 3D culture conditions. RNA sequencing and bioinformatic analyses of the differentially expressed genes (DEGs) using an ingenuity pathway analysis (IPA) suggested that various modulatory factors related to epithelial –mesenchymal transition (EMT) including STAT3, GLI1, ZNF367, NKX3-2, ZIC2, IFIT2, HEY1 and FBLX, may be the possible upstream regulators and/or causal network master regulators responsible for the acquirement of drug resistance in MIA PaCa-2-GR and -PR. In addition, among the prominently altered DEGs (Log2 fold changes more than 6 or less than −6), FABP5, IQSEC3, and GASK1B were identified as unique genes associated with their antisense RNA or pseudogenes, and among these, FABP5 and GASK1B are known to function as modulators of cancerous EMT. Therefore, the observations reported herein suggest that modulations of cancerous EMT may be key molecular mechanisms that are responsible for inducing chemoresistance against GEM or PTX in MIA PaCa-2 cells. Full article
(This article belongs to the Special Issue Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives 2nd Edition)
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Review

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15 pages, 1319 KiB  
Review
How Does Cancer Occur? How Should It Be Treated? Treatment from the Perspective of Alkalization Therapy Based on Science-Based Medicine
by Reo Hamaguchi, Masahide Isowa, Ryoko Narui, Hiromasa Morikawa, Toshihiro Okamoto and Hiromi Wada
Biomedicines 2024, 12(10), 2197; https://doi.org/10.3390/biomedicines12102197 - 26 Sep 2024
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Abstract
This review article investigates the relationship between mitochondrial dysfunction and cancer progression, emphasizing the metabolic shifts that promote tumor growth. Mitochondria are crucial for cellular energy production, but they also play a significant role in cancer progression by promoting glycolysis even under oxygen-rich [...] Read more.
This review article investigates the relationship between mitochondrial dysfunction and cancer progression, emphasizing the metabolic shifts that promote tumor growth. Mitochondria are crucial for cellular energy production, but they also play a significant role in cancer progression by promoting glycolysis even under oxygen-rich conditions, a phenomenon known as the Warburg effect. This metabolic reprogramming enables cancer cells to maintain an alkaline internal pH and an acidic external environment, which are critical for their proliferation and survival in hypoxic conditions. The article also explores the acidic tumor microenvironment (TME), a consequence of intensive glycolytic activity and proton production by cancer cells. This acidic milieu enhances the invasiveness and metastatic potential of cancer cells and contributes to increased resistance to chemotherapy. Alkalization therapy, which involves neutralizing this acidity through dietary modifications and the administration of alkalizing agents such as sodium bicarbonate, is highlighted as an effective strategy to counteract these adverse conditions and impede cancer progression. Integrating insights from science-based medicine, the review evaluates the effectiveness of alkalization therapy across various cancer types through clinical assessments. Science-based medicine, which utilizes inductive reasoning from observed clinical outcomes, lends support to the hypothesis of metabolic reprogramming in cancer treatment. By addressing both metabolic and environmental disruptions, this review suggests that considering cancer as primarily a metabolic disorder could lead to more targeted and effective treatment strategies, potentially improving outcomes for patients with advanced-stage cancers. Full article
(This article belongs to the Special Issue Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives 2nd Edition)
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