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Cells
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Cancer Therapy Based on Oxidative Stress Modulation
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Cancer Therapy Based on Oxidative Stress Modulation

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (15 September 2021) | Viewed by 16824

Special Issue Editors

Dr. Maria Condello

E-Mail Website
Guest Editor
National Center for Drug Research and Evaluation, National Institute of Health, Viale Regina Elena, 00161 Rome, Italy
Interests: characterization of multidrug-resistant tumor cells; in vitro study of apoptosis induced by chemotherapeutic drugs; in vitro study of autophagy (cell survival mechanism or type II programmed cell death); in vitro study of new anticancer strategies based on the use of natural products in combination with drugs, on electrochemotherapy, and on liposomes; study of interaction between cells and metal nanoparticles (ZnO or Ag-NPs) to investigate nanotoxicology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Stefania Meschini

E-Mail Website
Guest Editor
National Center for Drug Research and Evaluation, National Institute of Health, Viale Regina Elena, 00161 Rome, Italy
Interests: ultrastructural pathology; nanomedicine; nanotoxicology; cell biology; anticancer therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Reactive oxygen species represent a group of highly reactive molecules involved as regulators of important signaling pathways. Moderate levels of ROS are required for several cellular functions, such as cell proliferation and differentiation. When the production of ROS increases or scavenged ROS decreases, cells undergo oxidative stress. Consequently, ROS can contribute to many pathological conditions, such as cancer. Several hall markers of tumor cells, such as cell transformation, genome instability, hyperproliferation, immortalization, angiogenesis, epithelial–mesenchymal transition, and metastasis are influenced in several ways by intracellular ROS. Moreover, many chemotherapeutic drugs and radiotherapy used in anticancer therapy induce oxidative stress. The induction of apoptosis (Type I programmed cell death) by elevated ROS levels was the main mechanism responsible for the positive effects of targeted cancer therapy based on monoclonal antibodies and tyrosine kinase inhibitors. Recently, a new therapeutic approach to kill cancer cells is based on autophagy (Type II programmed cell death) induced by ROS. Finally, increased ROS levels impair multidrug resistance of cancer cells mediated by ATP transporters, which causes cancer development and metastasis.

This Special Issue is based on the complex interconnection between ROS levels and cancer, essentially based on the balance between ROS production and scavenging. Its aim is to depict the development of anticancer therapy based on modulating intracellular ROS levels to treat cancer.

Dr. Maria Condello
Prof. Stefania Meschini
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. Cells 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 2700 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

  • Reactive oxygen species
  • Cancer therapy
  • Apoptosis
  • Autophagy
  • Multidrug resistance

Published Papers (5 papers)

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Research

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22 pages, 3390 KiB  
Article
3,3′-Diindolylmethane Suppresses the Growth of Hepatocellular Carcinoma by Regulating Its Invasion, Migration, and ER Stress-Mediated Mitochondrial Apoptosis
by Suvesh Munakarmi, Juna Shrestha, Hyun-Beak Shin, Geum-Hwa Lee and Yeon-Jun Jeong
Cells 2021, 10(5), 1178; https://doi.org/10.3390/cells10051178 - 12 May 2021
Cited by 17 | Viewed by 3397
Abstract
Hepatocellular carcinoma (HCC) is the leading cause of cancer-related death worldwide with limited treatment options. Biomarker-based active phenolic flavonoids isolated from medicinal plants might shed some light on potential therapeutics for treating HCC. 3,3′-diindolylmethane (DIM) is a unique biologically active dimer of indole-3-carbinol [...] Read more.
Hepatocellular carcinoma (HCC) is the leading cause of cancer-related death worldwide with limited treatment options. Biomarker-based active phenolic flavonoids isolated from medicinal plants might shed some light on potential therapeutics for treating HCC. 3,3′-diindolylmethane (DIM) is a unique biologically active dimer of indole-3-carbinol (I3C), a phytochemical compound derived from Brassica species of cruciferous vegetables—such as broccoli, kale, cabbage, and cauliflower. It has anti-cancer effects on various cancers such as breast cancer, prostate cancer, endometrial cancer, and colon cancer. However, the molecular mechanism of DIM involved in reducing cancer risk and/or enhancing therapy remains unknown. The aim of the present study was to evaluate anti-cancer and therapeutic effects of DIM in human hepatoma cell lines Hep3B and HuhCell proliferation was measured with MTT and trypan blue colony formation assays. Migration, invasion, and apoptosis were measured with Transwell assays and flow cytometry analyses. Reactive oxygen species (ROS) intensity and the loss in mitochondrial membrane potential of Hep3B and Huh7 cells were determined using dihydroethidium (DHE) staining and tetramethylrhodamine ethyl ester dye. Results showed that DIM significantly suppressed HCC cell growth, proliferation, migration, and invasion in a concentration-dependent manner. Furthermore, DIM treatment activated caspase-dependent apoptotic pathway and suppressed epithelial–mesenchymal transition (EMT) via ER stress and unfolded protein response (UPR). Taken together, our results suggest that DIM is a potential anticancer drug for HCC therapy by targeting ER-stress/UPR. Full article
(This article belongs to the Special Issue Cancer Therapy Based on Oxidative Stress Modulation)
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Review

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17 pages, 7342 KiB  
Review
Role of Natural Antioxidant Products in Colorectal Cancer Disease: A Focus on a Natural Compound Derived from Prunus spinosa, Trigno Ecotype
by Maria Condello and Stefania Meschini
Cells 2021, 10(12), 3326; https://doi.org/10.3390/cells10123326 - 26 Nov 2021
Cited by 15 | Viewed by 2561
Abstract
Colorectal cancer (CRC) is on the rise in industrialized countries, which is why it is important to find new compounds that are effective, with little or no adverse health effects. CRC arises from some cells of the epithelium which, following a series of [...] Read more.
Colorectal cancer (CRC) is on the rise in industrialized countries, which is why it is important to find new compounds that are effective, with little or no adverse health effects. CRC arises from some cells of the epithelium which, following a series of genetic or epigenetic mutations, obtain a selective advantage. This work consists of a review on endogenous and exogenous antioxidant products that may have an efficacy in the treatment of CRC and an experimental study, in which the treatment was carried out with a natural compound with antitumor and antiproliferative activity, Prunus spinosa Trigno ecotype, patented by us, on HCT116 colorectal carcinoma cell line. The superoxide content was quantified after the treatments at different concentrations (2, 5, or 10 mg/mL) by means of the DHR123 probe; loss of the mitochondrial membrane potential with the tetramethylrodamine methyl ester (TMRM) cationic probe and reduced glutathione content (GSH) from monochlorobimane (MCB). This study revealed the importance of a careful choice of the concentration of the natural compound to be used in the CRC, due to the presence of a paradoxical effect, both antioxidant and pro-oxidant, depending on the different physiological conditions of the cell. Full article
(This article belongs to the Special Issue Cancer Therapy Based on Oxidative Stress Modulation)
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15 pages, 2252 KiB  
Review
Redox Sensitive Cysteine Residues as Crucial Regulators of Wild-Type and Mutant p53 Isoforms
by Elena Butturini, Giovanna Butera, Raffaella Pacchiana, Alessandra Carcereri de Prati, Sofia Mariotto and Massimo Donadelli
Cells 2021, 10(11), 3149; https://doi.org/10.3390/cells10113149 - 12 Nov 2021
Cited by 10 | Viewed by 2455
Abstract
The wild-type protein p53 plays a key role in preventing the formation of neoplasms by controlling cell growth. However, in more than a half of all cancers, the TP53 gene has missense mutations that appear during tumorigenesis. In most cases, the mutated gene [...] Read more.
The wild-type protein p53 plays a key role in preventing the formation of neoplasms by controlling cell growth. However, in more than a half of all cancers, the TP53 gene has missense mutations that appear during tumorigenesis. In most cases, the mutated gene encodes a full-length protein with the substitution of a single amino acid, resulting in structural and functional changes and acquiring an oncogenic role. This dual role of the wild-type protein and the mutated isoforms is also evident in the regulation of the redox state of the cell, with antioxidant and prooxidant functions, respectively. In this review, we introduce a new concept of the p53 protein by discussing its sensitivity to the cellular redox state. In particular, we focus on the discussion of structural and functional changes following post-translational modifications of redox-sensitive cysteine residues, which are also responsible for interacting with zinc ions for proper structural folding. We will also discuss therapeutic opportunities using small molecules targeting cysteines capable of modifying the structure and function of the p53 mutant isoforms in view of possible anticancer therapies for patients possessing the mutation in the TP53 gene. Full article
(This article belongs to the Special Issue Cancer Therapy Based on Oxidative Stress Modulation)
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19 pages, 1478 KiB  
Review
Autophagy and the Lysosomal System in Cancer
by Suresh Kumar, Miguel Sánchez-Álvarez, Fidel-Nicolás Lolo, Flavia Trionfetti, Raffaele Strippoli and Marco Cordani
Cells 2021, 10(10), 2752; https://doi.org/10.3390/cells10102752 - 14 Oct 2021
Cited by 24 | Viewed by 4000
Abstract
Autophagy and the lysosomal system, together referred to as the autophagolysosomal system, is a cellular quality control network which maintains cellular health and homeostasis by removing cellular waste including protein aggregates, damaged organelles, and invading pathogens. As such, the autophagolysosomal system has roles [...] Read more.
Autophagy and the lysosomal system, together referred to as the autophagolysosomal system, is a cellular quality control network which maintains cellular health and homeostasis by removing cellular waste including protein aggregates, damaged organelles, and invading pathogens. As such, the autophagolysosomal system has roles in a variety of pathophysiological disorders, including cancer, neurological disorders, immune- and inflammation-related diseases, and metabolic alterations, among others. The autophagolysosomal system is controlled by TFEB, a master transcriptional regulator driving the expression of multiple genes, including autophagoly sosomal components. Importantly, Reactive Oxygen Species (ROS) production and control are key aspects of the physiopathological roles of the autophagolysosomal system, and may hold a key for synergistic therapeutic interventions. In this study, we reviewed our current knowledge on the biology and physiopathology of the autophagolysosomal system, and its potential for therapeutic intervention in cancer. Full article
(This article belongs to the Special Issue Cancer Therapy Based on Oxidative Stress Modulation)
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13 pages, 5595 KiB  
Review
Metabolic Stress Adaptations Underlie Mammary Gland Morphogenesis and Breast Cancer Progression
by Chun-Chao Wang
Cells 2021, 10(10), 2641; https://doi.org/10.3390/cells10102641 - 02 Oct 2021
Cited by 4 | Viewed by 3292
Abstract
Breast cancers display dynamic reprogrammed metabolic activities as cancers develop from premalignant lesions to primary tumors, and then metastasize. Numerous advances focus on how tumors develop pro-proliferative metabolic signaling that differs them from adjacent, non-transformed epithelial tissues. This leads to targetable oncogene-driven liabilities [...] Read more.
Breast cancers display dynamic reprogrammed metabolic activities as cancers develop from premalignant lesions to primary tumors, and then metastasize. Numerous advances focus on how tumors develop pro-proliferative metabolic signaling that differs them from adjacent, non-transformed epithelial tissues. This leads to targetable oncogene-driven liabilities among breast cancer subtypes. Other advances demonstrate how microenvironments trigger stress-response at single-cell resolution. Microenvironmental heterogeneities give rise to cell regulatory states in cancer cell spheroids in three-dimensional cultures and at stratified terminal end buds during mammary gland morphogenesis, where stress and survival signaling juxtapose. The cell-state specificity in stress signaling networks recapture metabolic evolution during cancer progression. Understanding lineage-specific metabolic phenotypes in experimental models is useful for gaining a deeper understanding of subtype-selective breast cancer metabolism. Full article
(This article belongs to the Special Issue Cancer Therapy Based on Oxidative Stress Modulation)
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