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Cancer and Stresses
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Cancer and Stresses

A special issue of Stresses (ISSN 2673-7140). This special issue belongs to the section "Animal and Human Stresses".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 15455

Special Issue Editors

Prof. Dr. David R. Wallace

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Guest Editor
Department of Pharmacology & Physiology, School of Biomedical Science, Oklahoma State University Center for Health Sciences, Tulsa, OK 74107-1898, USA
Interests: pancreatic cancer; environmental toxicants; mitochondrial toxicity; apoptosis; cellular regulation; tryptophan-kynurenine pathway; indoleamine 2,3-dioxygenase
Special Issues, Collections and Topics in MDPI journals
Dr. Pinar Uysal Onganer

E-Mail Website
Guest Editor
Cancer Research Group, School of Life Sciences, College of Liberal Arts & Sciences, University of Westminster, London, UK
Interests: cancer biology; metastasis; non-coding RNAs; cancer stem cells
Special Issues, Collections and Topics in MDPI journals
Dr. Aleksandra Buha Đorđević

E-Mail Website
Guest Editor
Department of Toxicology “Akademik Danilo Soldatović”, University of Belgrade-Faculty of Pharmacy, 11000 Belgrade, Serbia
Interests: toxicology; endocrine disrupting chemicals; mixtures; human health risk assessment; chemical carcinogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is a heterogeneous disease that promotes cell growth, disables cell death mechanisms, and evades immune surveillance and therapy. Metabolic stress is a common occurrence in human tumours and is caused by multiple factors. The tumour-mediated metabolic stress response is linked to both apoptosis and autophagy, and understanding these pathways is essential for developing cancer therapies. In this Special Issue of Stresses, our objective is to explore the mechanisms of cellular stresses in cancer prognosis and treatment. Cells can respond to stress in various ways, ranging from the activation of survival pathways to the initiation of cell death that eventually eliminates damaged cells. Potential topics regarding cancer development include the molecular mechanisms underlying oxidative stress, DNA damage, immune evasion, apoptosis, use of antioxidants as combination therapy, and potential cellular stress biomarkers. Authors are invited to submit original research papers, reviews, and short communications.

Prof. Dr. David R. Wallace
Dr. Pinar Uysal Onganer
Dr. Aleksandra Buha Đorđević
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. Stresses is an international peer-reviewed open access quarterly 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 1000 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

  • cancer
  • mitochondria
  • DNA damage
  • apoptosis
  • oxidative stress
  • cellular stress
  • antioxidants
  • autophagy
  • inflammation
  • cytokines
  • chemokines
  • mutagenicity and genotoxicity

Published Papers (4 papers)

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Research

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11 pages, 1151 KiB  
Article
Phytochemical and In Vitro Cytotoxic Screening of Chloroform Extract of Ehretia microphylla Lamk
by Pooja Sharma, Richa Shri and Suresh Kumar
Stresses 2022, 2(4), 384-394; https://0-doi-org.brum.beds.ac.uk/10.3390/stresses2040027 - 03 Oct 2022
Cited by 1 | Viewed by 3246
Abstract
Ehretia microphylla of the Boraginaceae family has been extensively used as a folklore remedy for the treatment of a wide range of ailments such as cough, cancer, allergies, and gastrointestinal and venereal disorders. Extensive literature review reports have revealed these findings due to [...] Read more.
Ehretia microphylla of the Boraginaceae family has been extensively used as a folklore remedy for the treatment of a wide range of ailments such as cough, cancer, allergies, and gastrointestinal and venereal disorders. Extensive literature review reports have revealed these findings due to the presence of numerous phytomolecules. To validate traditional claims for cytotoxic activity of E. microphylla, the present study was undertaken. Dried leaves of the plant were powdered and defatted with petroleum ether followed by hot continuous extraction with chloroform. The chloroform extract was subjected to in vitro cytotoxic screening against a panel of human cancer cell lines such as HCT-116 (colon), MCF-7 (breast), PC-3 (prostate), A-549 (lung), HL-60 (leukemia) and MiaPaCa-2 (pancreatic) at 50 µM using SRB assay. The extract exhibited noteworthy cytotoxicity activity against breast and lung cancer. It exhibited 85.55% and 77.93% inhibition against MCF-7 and A-549 cancer cell lines, respectively. The mechanism behind cell death was determined using the DAPI staining method, which induces alteration in nuclear morphology in MCF-7 cell lines evidenced through DAPI staining. Phytochemical screening of E. microphylla extract showed the presence of saponins, steroids, lipids, tannins and triterpenoids. The chemoprofile of the chloroform extract of E. microphylla leaves was established using an n-hexane:ethyl acetate solvent system in a ratio of 6:4. The developed chromatogram showed five spots both in visible and UV light at 254 nm. The information provided in the present study will enable further studies on the isolation and characterization of bioactive compounds/fractions by following bioactivity-guided fractionation, and thus, the plant has the potential to reduce proliferation and may induce cell death via apoptosis in breast cancer cells. Full article
(This article belongs to the Special Issue Cancer and Stresses)
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12 pages, 1810 KiB  
Article
Aberrant Expression of ZIP and ZnT Zinc Transporters in UROtsa Cells Transformed to Malignant Cells by Cadmium
by Soisungwan Satarug, Scott H. Garrett, Seema Somji, Mary Ann Sens and Donald A. Sens
Stresses 2021, 1(2), 78-89; https://0-doi-org.brum.beds.ac.uk/10.3390/stresses1020007 - 22 Apr 2021
Cited by 7 | Viewed by 2952
Abstract
Maintenance of zinc homeostasis is pivotal to the regulation of cell growth, differentiation, apoptosis, and defense mechanisms. In mammalian cells, control of cellular zinc homeostasis is through zinc uptake, zinc secretion, and zinc compartmentalization, mediated by metal transporters of the Zrt-/Irt-like protein (ZIP) [...] Read more.
Maintenance of zinc homeostasis is pivotal to the regulation of cell growth, differentiation, apoptosis, and defense mechanisms. In mammalian cells, control of cellular zinc homeostasis is through zinc uptake, zinc secretion, and zinc compartmentalization, mediated by metal transporters of the Zrt-/Irt-like protein (ZIP) family and the Cation Diffusion Facilitators (CDF) or ZnT family. We quantified transcript levels of ZIP and ZnT zinc transporters expressed by non-tumorigenic UROtsa cells and compared with those expressed by UROtsa clones that were experimentally transformed to cancer cells by prolonged exposure to cadmium (Cd). Although expression of the ZIP8 gene in parent UROtsa cells was lower than ZIP14 (0.1 vs. 83 transcripts per 1000 β-actin transcripts), an increased expression of ZIP8 concurrent with a reduction in expression of one or two zinc influx transporters, namely ZIP1, ZIP2, and ZIP3, were seen in six out of seven transformed UROtsa clones. Aberrant expression of the Golgi zinc transporters ZIP7, ZnT5, ZnT6, and ZnT7 were also observed. One transformed clone showed distinctively increased expression of ZIP6, ZIP10, ZIP14, and ZnT1, with a diminished ZIP8 expression. These data suggest intracellular zinc dysregulation and aberrant zinc homeostasis both in the cytosol and in the Golgi in the transformed UROtsa clones. These results provide evidence for zinc dysregulation in transformed UROtsa cells that may contribute in part to their malignancy and/or muscle invasiveness. Full article
(This article belongs to the Special Issue Cancer and Stresses)
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Review

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16 pages, 355 KiB  
Review
Evidence for Ovarian and Testicular Toxicities of Cadmium and Detoxification by Natural Substances
by Martin Massányi, Soisungwan Satarug, Roberto Madeddu, Robert Stawarz and Peter Massányi
Stresses 2022, 2(1), 1-16; https://0-doi-org.brum.beds.ac.uk/10.3390/stresses2010001 - 22 Dec 2021
Cited by 6 | Viewed by 3395
Abstract
Cadmium (Cd) is an environmental toxicant, capable of reducing mitochondrial ATP production and promoting the formation of reactive oxygen species (ROS) with resultant oxidative stress conditions. The ovary and testis are the primary gonads in which female gametes (oocytes) and male gametes (spermatozoa), [...] Read more.
Cadmium (Cd) is an environmental toxicant, capable of reducing mitochondrial ATP production and promoting the formation of reactive oxygen species (ROS) with resultant oxidative stress conditions. The ovary and testis are the primary gonads in which female gametes (oocytes) and male gametes (spermatozoa), estrogen and testosterone are produced. These organs are particularly susceptible to Cd cytotoxicity due to their high metabolic activities and high energy demands. In this review, epidemiological and experimental studies examining Cd toxicities in gonads are highlighted together with studies using zinc (Zn), selenium (Se), and natural substances to reduce the effects of Cd on follicular genesis and spermatogenesis. Higher blood concentrations of Cd ([Cd]b) were associated with longer time-to-pregnancy in a prospective cohort study. Cd excretion rate (ECd) as low as 0.8 μg/g creatinine was associated with reduced spermatozoa vitality, while Zn and Se may protect against spermatozoa quality decline accompanying Cd exposure. ECd > 0.68 µg/g creatinine were associated with an increased risk of premature ovarian failure by 2.5-fold, while [Cd]b ≥ 0.34 µg/L were associated with a 2.5-fold increase in the risk of infertility in women. Of concern, urinary excretion of Cd at 0.68 and 0.8 μg/g creatinine found to be associated with fecundity are respectively 13% and 15% of the conventional threshold limit for Cd-induced kidney tubular effects of 5.24 μg/g creatinine. These findings suggest that toxicity of Cd in primary reproductive organs occurs at relatively low body burden, thereby arguing for minimization of exposure and environmental pollution by Cd and its transfer to the food web. Full article
(This article belongs to the Special Issue Cancer and Stresses)
18 pages, 756 KiB  
Review
MicroRNA-Regulated Signaling Pathways: Potential Biomarkers for Pancreatic Ductal Adenocarcinoma
by Maria Mortoglou, David Wallace, Aleksandra Buha Djordjevic, Vladimir Djordjevic, E. Damla Arisan and Pinar Uysal-Onganer
Stresses 2021, 1(1), 30-47; https://0-doi-org.brum.beds.ac.uk/10.3390/stresses1010004 - 10 Mar 2021
Cited by 13 | Viewed by 4257
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is the most aggressive and invasive type of pancreatic cancer (PCa) and is expected to be the second most common cause of cancer-associated deaths. The high mortality rate is due to the asymptomatic progression of the clinical features until [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is the most aggressive and invasive type of pancreatic cancer (PCa) and is expected to be the second most common cause of cancer-associated deaths. The high mortality rate is due to the asymptomatic progression of the clinical features until the advanced stages of the disease and the limited effectiveness of the current therapeutics. Aberrant expression of several microRNAs (miRs/miRNAs) has been related to PDAC progression and thus they could be potential early diagnostic, prognostic, and/or therapeutic predictors for PDAC. miRs are small (18 to 24 nucleotides long) non-coding RNAs, which regulate the expression of key genes by targeting their 3′-untranslated mRNA region. Increased evidence has also suggested that the chemoresistance of PDAC cells is associated with metabolic alterations. Metabolic stress and the dysfunctionality of systems to compensate for the altered metabolic status of PDAC cells is the foundation for cellular damage. Current data have implicated multiple systems as hallmarks of PDAC development, such as glutamine redox imbalance, oxidative stress, and mitochondrial dysfunction. Hence, both the aberrant expression of miRs and dysregulation in metabolism can have unfavorable effects in several biological processes, such as apoptosis, cell proliferation, growth, survival, stress response, angiogenesis, chemoresistance, invasion, and migration. Therefore, due to these dismal statistics, it is crucial to develop beneficial therapeutic strategies based on an improved understanding of the biology of both miRs and metabolic mediators. This review focuses on miR-mediated pathways and therapeutic resistance mechanisms in PDAC and evaluates the impact of metabolic alterations in the progression of PDAC. Full article
(This article belongs to the Special Issue Cancer and Stresses)
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