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Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology
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Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 October 2019) | Viewed by 88494

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editors

Dr. Antonella Fioravanti

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Guest Editor
Sbarro Institute for Cancer Research and Molecular Medicine and Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
Interests: osteoarthritis; rheumatic diseases; microRNA; psoriatic arthritis; rheumatoid arthritis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Francesco Dotta

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Guest Editor
Diabetes Unit, Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Antonio Giordano

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Guest Editor
1. Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
2. Department of Medical Biotechnologies, University of Siena, Siena, Italy
Interests: cell cycle; tumor suppressor genes; RB family; CDK inhibitors; environment and cancer
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Luigi Pirtoli

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Guest Editor
Department of Biology, College of Science and Technology, Temple University, Philadelphia, PA, USA
Interests: oncology; radiobiology; radiotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

MicroRNAs (miRNAs)—small non-coding RNAs 19–24 nucleotides long—have emerged as important post-transcriptional regulators of gene expression, by binding specific sequences within target messenger RNA (mRNA). The importance of miRNA epigenetic regulation in cellular function is becoming increasingly clear as novel targets are discovered. They have been associated with controlling important cellular processes, such as lipid metabolism, apoptosis, differentiation, and organ development. Importantly, miRNAs have recently been addressed as novel mediators of cell–cell communication being cell secreted, and are found in many different biological fluids. Such characteristics also make miRNA potential disease biomarkers.

An altered miRNA expression has been linked to pathological features, such as inflammatory, degenerative, or autoimmune processes, and is involved in several disease outcomes, including cancer, cardiovascular diseases, diabetes mellitus, and rheumatic and neurological disorders.

Although they have been extensively studied, their detailed mechanisms are not yet fully understood.

Reactive oxygen species (ROS) are free radicals containing oxygen molecules derived from cellular oxidative metabolism, including enzyme activities and mitochondrial respiration, and play a pivotal role in many cellular functions. Whereas ROS are essential for normal cellular processes, the aberrant production of ROS, or the failure of the capacity to scavenge excessive ROS, determines an altered redox status with an excessive synthesis of free radicals, leading to an imbalance in the redox environment of the cell.

The loss of normal ROS levels can cause the damage of lipids, proteins, and DNA, all of which contribute to the development of various pathologies such as neurological disorders, rheumatic and cardiovascular diseases, diabetes, and cancer.

Recent research highlights conditions where there is a cross-talk between miRNA and oxidative stress, even if this complex and mutual interaction needs to be amply elucidated.

In this regard, we invite investigators to contribute original research articles and review articles that will stimulate the continuing efforts to understand the mechanisms underlying the interaction between miRNA and oxidative stress under normal and diseased processes, to develop strategies to treat these pathological conditions and to identify novel biomarkers of disease.

Dr. Antonella Fioravanti
Prof. Dr. Francesco Dotta
Prof. Dr. Antonio Giordano
Prof. Dr. Luigi Pirtoli
Guest Editors

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Keywords

  • microRNA
  • oxidative stress
  • cardiovascular diseases
  • rheumatic diseases
  • cancer
  • diabetes
  • neurological disorders
  • multiple sclerosis

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Published Papers (15 papers)

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Editorial

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3 pages, 186 KiB  
Editorial
Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology
by Antonella Fioravanti, Luigi Pirtoli, Antonio Giordano and Francesco Dotta
Int. J. Mol. Sci. 2020, 21(4), 1270; https://doi.org/10.3390/ijms21041270 - 13 Feb 2020
Cited by 11 | Viewed by 2261
Abstract
MicroRNAs (miRNA), are short regulatory RNA molecules that regulate gene expression by binding specific sequences within target messenger RNA (mRNA) [...] Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)

Research

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37 pages, 8520 KiB  
Article
MicroRNA Mediate Visfatin and Resistin Induction of Oxidative Stress in Human Osteoarthritic Synovial Fibroblasts Via NF-κB Pathway
by Sara Cheleschi, Ines Gallo, Marcella Barbarino, Stefano Giannotti, Nicola Mondanelli, Antonio Giordano, Sara Tenti and Antonella Fioravanti
Int. J. Mol. Sci. 2019, 20(20), 5200; https://doi.org/10.3390/ijms20205200 - 20 Oct 2019
Cited by 35 | Viewed by 4502
Abstract
Synovial membrane inflammation actively participate to structural damage during osteoarthritis (OA). Adipokines, miRNA, and oxidative stress contribute to synovitis and cartilage destruction in OA. We investigated the relationship between visfatin, resistin and miRNA in oxidative stress regulation, in human OA synovial fibroblasts. Cultured [...] Read more.
Synovial membrane inflammation actively participate to structural damage during osteoarthritis (OA). Adipokines, miRNA, and oxidative stress contribute to synovitis and cartilage destruction in OA. We investigated the relationship between visfatin, resistin and miRNA in oxidative stress regulation, in human OA synovial fibroblasts. Cultured cells were treated with visfatin and resistin. After 24 h, we evaluated various pro-inflammatory cytokines, metalloproteinases (MMPs), type II collagen (Col2a1), miR-34a, miR-146a, miR-181a, antioxidant enzymes, and B-cell lymphoma (BCL)2 by qRT-PCR, apoptosis and mitochondrial superoxide production by cytometry, p50 nuclear factor (NF)-κB by immunofluorescence. Synoviocytes were transfected with miRNA inhibitors and oxidative stress evaluation after adipokines stimulus was performed. The implication of NF-κB pathway was assessed by the use of a NF-κB inhibitor (BAY-11-7082). Visfatin and resistin significantly up-regulated gene expression of interleukin (IL)-1β, IL-6, IL-17, tumor necrosis factor (TNF)-α, MMP-1, MMP-13 and reduced Col2a1. Furthermore, adipokines induced apoptosis and superoxide production, the transcriptional levels of BCL2, superoxide dismutase (SOD)-2, catalase (CAT), nuclear factor erythroid 2 like 2 (NRF2), miR-34a, miR-146a, and miR-181a. MiRNA inhibitors counteracted adipokines modulation of oxidative stress. Visfatin and resistin effects were suppressed by BAY-11-7082. Our data suggest that miRNA may represent possible mediators of oxidative stress induced by visfatin and resistin via NF-κB pathway in human OA synoviocytes. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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21 pages, 4423 KiB  
Article
miR526b and miR655 Induce Oxidative Stress in Breast Cancer
by Bonita Shin, Riley Feser, Braydon Nault, Stephanie Hunter, Sujit Maiti, Kingsley Chukwunonso Ugwuagbo and Mousumi Majumder
Int. J. Mol. Sci. 2019, 20(16), 4039; https://doi.org/10.3390/ijms20164039 - 19 Aug 2019
Cited by 33 | Viewed by 7620
Abstract
In eukaryotes, overproduction of reactive oxygen species (ROS) causes oxidative stress, which contributes to chronic inflammation and cancer. MicroRNAs (miRNAs) are small, endogenously produced RNAs that play a major role in cancer progression. We established that overexpression of miR526b/miR655 promotes aggressive breast cancer [...] Read more.
In eukaryotes, overproduction of reactive oxygen species (ROS) causes oxidative stress, which contributes to chronic inflammation and cancer. MicroRNAs (miRNAs) are small, endogenously produced RNAs that play a major role in cancer progression. We established that overexpression of miR526b/miR655 promotes aggressive breast cancer phenotypes. Here, we investigated the roles of miR526b/miR655 in oxidative stress in breast cancer using in vitro and in silico assays. miRNA-overexpression in MCF7 cells directly enhances ROS and superoxide (SO) production, detected with fluorescence assays. We found that cell-free conditioned media contain extracellular miR526b/miR655 and treatment with these miRNA-conditioned media causes overproduction of ROS/SO in MCF7 and primary cells (HUVECs). Thioredoxin Reductase 1 (TXNRD1) is an oxidoreductase that maintains ROS/SO concentration. Overexpression of TXNRD1 is associated with breast cancer progression. We observed that miR526b/miR655 overexpression upregulates TXNRD1 expression in MCF7 cells, and treatment with miRNA-conditioned media upregulates TXNRD1 in both MCF7 and HUVECs. Bioinformatic analysis identifies two negative regulators of TXNRD1, TCF21 and PBRM1, as direct targets of miR526b/miR655. We validated that TCF21 and PBRM1 were significantly downregulated with miRNA upregulation, establishing a link between miR526b/miR655 and TXNRD1. Finally, treatments with oxidative stress inducers such as H2O2 or miRNA-conditioned media showed an upregulation of miR526b/miR655 expression in MCF7 cells, indicating that oxidative stress also induces miRNA overexpression. This study establishes the dynamic functions of miR526b/miR655 in oxidative stress induction in breast cancer. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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13 pages, 2230 KiB  
Article
miR-27a-5p Attenuates Hypoxia-induced Rat Cardiomyocyte Injury by Inhibiting Atg7
by Jinwei Zhang, Wanling Qiu, Jideng Ma, Yujie Wang, Zihui Hu, Keren Long, Xun Wang, Long Jin, Qianzi Tang, Guoqing Tang, Li Zhu, Xuewei Li, Surong Shuai and Mingzhou Li
Int. J. Mol. Sci. 2019, 20(10), 2418; https://doi.org/10.3390/ijms20102418 - 16 May 2019
Cited by 32 | Viewed by 4159
Abstract
Acute myocardial infarction (AMI) is an ischemic heart disease with high mortality worldwide. AMI triggers a hypoxic microenvironment and induces extensive myocardial injury, including autophagy and apoptosis. MiRNAs, which are a class of posttranscriptional regulators, have been shown to be involved in the [...] Read more.
Acute myocardial infarction (AMI) is an ischemic heart disease with high mortality worldwide. AMI triggers a hypoxic microenvironment and induces extensive myocardial injury, including autophagy and apoptosis. MiRNAs, which are a class of posttranscriptional regulators, have been shown to be involved in the development of ischemic heart diseases. We have previously reported that hypoxia significantly alters the miRNA transcriptome in rat cardiomyoblast cells (H9c2), including miR-27a-5p. In the present study, we further investigated the potential function of miR-27a-5p in the cardiomyocyte response to hypoxia, and showed that miR-27a-5p expression was downregulated in the H9c2 cells at different hypoxia-exposed timepoints and the myocardium of a rat AMI model. Follow-up experiments revealed that miR-27a-5p attenuated hypoxia-induced cardiomyocyte injury by regulating autophagy and apoptosis via Atg7, which partly elucidated the anti-hypoxic injury effects of miR-27a-5p. Taken together, this study shows that miR-27a-5p has a cardioprotective effect on hypoxia-induced H9c2 cell injury, suggesting it may be a novel target for the treatment of hypoxia-related heart diseases. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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Review

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20 pages, 504 KiB  
Review
microRNAs Tune Oxidative Stress in Cancer Therapeutic Tolerance and Resistance
by Wen Cai Zhang
Int. J. Mol. Sci. 2019, 20(23), 6094; https://doi.org/10.3390/ijms20236094 - 3 Dec 2019
Cited by 19 | Viewed by 4891
Abstract
Relapsed disease following first-line therapy remains one of the central problems in cancer management, including chemotherapy, radiotherapy, growth factor receptor-based targeted therapy, and immune checkpoint-based immunotherapy. Cancer cells develop therapeutic resistance through both intrinsic and extrinsic mechanisms including cellular heterogeneity, drug tolerance, bypassing [...] Read more.
Relapsed disease following first-line therapy remains one of the central problems in cancer management, including chemotherapy, radiotherapy, growth factor receptor-based targeted therapy, and immune checkpoint-based immunotherapy. Cancer cells develop therapeutic resistance through both intrinsic and extrinsic mechanisms including cellular heterogeneity, drug tolerance, bypassing alternative signaling pathways, as well as the acquisition of new genetic mutations. Reactive oxygen species (ROSs) are byproducts originated from cellular oxidative metabolism. Recent discoveries have shown that a disabled antioxidant program leads to therapeutic resistance in several types of cancers. ROSs are finely tuned by dysregulated microRNAs, and vice versa. However, mechanisms of a crosstalk between ROSs and microRNAs in regulating therapeutic resistance are not clear. Here, we summarize how the microRNA–ROS network modulates cancer therapeutic tolerance and resistance and direct new vulnerable targets against drug tolerance and resistance for future applications. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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26 pages, 2948 KiB  
Review
Interplay between MicroRNAs and Oxidative Stress in Neurodegenerative Diseases
by Julia Konovalova, Dmytro Gerasymchuk, Ilmari Parkkinen, Piotr Chmielarz and Andrii Domanskyi
Int. J. Mol. Sci. 2019, 20(23), 6055; https://doi.org/10.3390/ijms20236055 - 30 Nov 2019
Cited by 143 | Viewed by 10553
Abstract
MicroRNAs are post-transcriptional regulators of gene expression, crucial for neuronal differentiation, survival, and activity. Age-related dysregulation of microRNA biogenesis increases neuronal vulnerability to cellular stress and may contribute to the development and progression of neurodegenerative diseases. All major neurodegenerative disorders are also associated [...] Read more.
MicroRNAs are post-transcriptional regulators of gene expression, crucial for neuronal differentiation, survival, and activity. Age-related dysregulation of microRNA biogenesis increases neuronal vulnerability to cellular stress and may contribute to the development and progression of neurodegenerative diseases. All major neurodegenerative disorders are also associated with oxidative stress, which is widely recognized as a potential target for protective therapies. Albeit often considered separately, microRNA networks and oxidative stress are inextricably entwined in neurodegenerative processes. Oxidative stress affects expression levels of multiple microRNAs and, conversely, microRNAs regulate many genes involved in an oxidative stress response. Both oxidative stress and microRNA regulatory networks also influence other processes linked to neurodegeneration, such as mitochondrial dysfunction, deregulation of proteostasis, and increased neuroinflammation, which ultimately lead to neuronal death. Modulating the levels of a relatively small number of microRNAs may therefore alleviate pathological oxidative damage and have neuroprotective activity. Here, we review the role of individual microRNAs in oxidative stress and related pathways in four neurodegenerative conditions: Alzheimer’s (AD), Parkinson’s (PD), Huntington’s (HD) disease, and amyotrophic lateral sclerosis (ALS). We also discuss the problems associated with the use of oversimplified cellular models and highlight perspectives of studying microRNA regulation and oxidative stress in human stem cell-derived neurons. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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Graphical abstract

25 pages, 1592 KiB  
Review
The Role of MicroRNAs in Diabetes-Related Oxidative Stress
by Mirza Muhammad Fahd Qadir, Dagmar Klein, Silvia Álvarez-Cubela, Juan Domínguez-Bendala and Ricardo Luis Pastori
Int. J. Mol. Sci. 2019, 20(21), 5423; https://doi.org/10.3390/ijms20215423 - 31 Oct 2019
Cited by 23 | Viewed by 5541
Abstract
Cellular stress, combined with dysfunctional, inadequate mitochondrial phosphorylation, produces an excessive amount of reactive oxygen species (ROS) and an increased level of ROS in cells, which leads to oxidation and subsequent cellular damage. Because of its cell damaging action, an association between anomalous [...] Read more.
Cellular stress, combined with dysfunctional, inadequate mitochondrial phosphorylation, produces an excessive amount of reactive oxygen species (ROS) and an increased level of ROS in cells, which leads to oxidation and subsequent cellular damage. Because of its cell damaging action, an association between anomalous ROS production and disease such as Type 1 (T1D) and Type 2 (T2D) diabetes, as well as their complications, has been well established. However, there is a lack of understanding about genome-driven responses to ROS-mediated cellular stress. Over the last decade, multiple studies have suggested a link between oxidative stress and microRNAs (miRNAs). The miRNAs are small non-coding RNAs that mostly suppress expression of the target gene by interaction with its 3’untranslated region (3′UTR). In this paper, we review the recent progress in the field, focusing on the association between miRNAs and oxidative stress during the progression of diabetes. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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Graphical abstract

21 pages, 1628 KiB  
Review
The Yin-Yang Regulation of Reactive Oxygen Species and MicroRNAs in Cancer
by Kamesh R. Babu and Yvonne Tay
Int. J. Mol. Sci. 2019, 20(21), 5335; https://doi.org/10.3390/ijms20215335 - 26 Oct 2019
Cited by 47 | Viewed by 6930
Abstract
Reactive oxygen species (ROS) are highly reactive oxygen-containing chemical species formed as a by-product of normal aerobic respiration and also from a number of other cellular enzymatic reactions. ROS function as key mediators of cellular signaling pathways involved in proliferation, survival, apoptosis, and [...] Read more.
Reactive oxygen species (ROS) are highly reactive oxygen-containing chemical species formed as a by-product of normal aerobic respiration and also from a number of other cellular enzymatic reactions. ROS function as key mediators of cellular signaling pathways involved in proliferation, survival, apoptosis, and immune response. However, elevated and sustained ROS production promotes tumor initiation by inducing DNA damage or mutation and activates oncogenic signaling pathways to promote cancer progression. Recent studies have shown that ROS can facilitate carcinogenesis by controlling microRNA (miRNA) expression through regulating miRNA biogenesis, transcription, and epigenetic modifications. Likewise, miRNAs have been shown to control cellular ROS homeostasis by regulating the expression of proteins involved in ROS production and elimination. In this review, we summarized the significance of ROS in cancer initiation, progression, and the regulatory crosstalk between ROS and miRNAs in cancer. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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24 pages, 1598 KiB  
Review
Interplay Between MicroRNAs and Oxidative Stress in Ovarian Conditions with a Focus on Ovarian Cancer and Endometriosis
by Josep Marí-Alexandre, Antonio Pellín Carcelén, Cristina Agababyan, Andrea Moreno-Manuel, Javier García-Oms, Silvia Calabuig-Fariñas and Juan Gilabert-Estellés
Int. J. Mol. Sci. 2019, 20(21), 5322; https://doi.org/10.3390/ijms20215322 - 25 Oct 2019
Cited by 33 | Viewed by 9362
Abstract
Ovarian cancer and endometriosis are two distinct gynaecological conditions that share many biological aspects incuding proliferation, invasion of surrounding tissue, inflammation, inhibition of apoptosis, deregulation of angiogenesis and the ability to spread at a distance. miRNAs are small non-coding RNAs (19–22 nt) that [...] Read more.
Ovarian cancer and endometriosis are two distinct gynaecological conditions that share many biological aspects incuding proliferation, invasion of surrounding tissue, inflammation, inhibition of apoptosis, deregulation of angiogenesis and the ability to spread at a distance. miRNAs are small non-coding RNAs (19–22 nt) that act as post-transcriptional modulators of gene expression and are involved in several of the aforementioned processes. In addition, a growing body of evidence supports the contribution of oxidative stress (OS) to these gynaecological diseases: increased peritoneal OS due to the decomposition of retrograde menstruation blood facilitates both endometriotic lesion development and fallopian tube malignant transformation leading to high-grade serous ovarian cancer (HGSOC). Furthermore, as HGSOC develops, increased OS levels are associated with chemoresistance. Finally, continued bleeding within ovarian endometrioma raises OS levels and contributes to the development of endometriosis-associated ovarian cancer (EAOC). Therefore, this review aims to address the need for a better understanding of the dialogue between miRNAs and oxidative stress in the pathophysiology of ovarian conditions: endometriosis, EAOC and HGSOC. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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24 pages, 1158 KiB  
Review
The Crosstalk of miRNA and Oxidative Stress in the Liver: From Physiology to Pathology and Clinical Implications
by Eckhard Klieser, Christian Mayr, Tobias Kiesslich, Till Wissniowski, Pietro Di Fazio, Daniel Neureiter and Matthias Ocker
Int. J. Mol. Sci. 2019, 20(21), 5266; https://doi.org/10.3390/ijms20215266 - 23 Oct 2019
Cited by 41 | Viewed by 4826
Abstract
The liver is the central metabolic organ of mammals. In humans, most diseases of the liver are primarily caused by an unhealthy lifestyle–high fat diet, drug and alcohol consumption- or due to infections and exposure to toxic substances like aflatoxin or other environmental [...] Read more.
The liver is the central metabolic organ of mammals. In humans, most diseases of the liver are primarily caused by an unhealthy lifestyle–high fat diet, drug and alcohol consumption- or due to infections and exposure to toxic substances like aflatoxin or other environmental factors. All these noxae cause changes in the metabolism of functional cells in the liver. In this literature review we focus on the changes at the miRNA level, the formation and impact of reactive oxygen species and the crosstalk between those factors. Both, miRNAs and oxidative stress are involved in the multifactorial development and progression of acute and chronic liver diseases, as well as in viral hepatitis and carcinogenesis, by influencing numerous signaling and metabolic pathways. Furthermore, expression patterns of miRNAs and antioxidants can be used for biomonitoring the course of disease and show potential to serve as possible therapeutic targets. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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24 pages, 501 KiB  
Review
Roles of Thyroid Hormone-Associated microRNAs Affecting Oxidative Stress in Human Hepatocellular Carcinoma
by Po-Shuan Huang, Chia-Siu Wang, Chau-Ting Yeh and Kwang-Huei Lin
Int. J. Mol. Sci. 2019, 20(20), 5220; https://doi.org/10.3390/ijms20205220 - 21 Oct 2019
Cited by 24 | Viewed by 4613
Abstract
Oxidative stress occurs as a result of imbalance between the generation of reactive oxygen species (ROS) and antioxidant genes in cells, causing damage to lipids, proteins, and DNA. Accumulating damage of cellular components can trigger various diseases, including metabolic syndrome and cancer. Over [...] Read more.
Oxidative stress occurs as a result of imbalance between the generation of reactive oxygen species (ROS) and antioxidant genes in cells, causing damage to lipids, proteins, and DNA. Accumulating damage of cellular components can trigger various diseases, including metabolic syndrome and cancer. Over the past few years, the physiological significance of microRNAs (miRNA) in cancer has been a focus of comprehensive research. In view of the extensive level of miRNA interference in biological processes, the roles of miRNAs in oxidative stress and their relevance in physiological processes have recently become a subject of interest. In-depth research is underway to specifically address the direct or indirect relationships of oxidative stress-induced miRNAs in liver cancer and the potential involvement of the thyroid hormone in these processes. While studies on thyroid hormone in liver cancer are abundantly documented, no conclusive information on the potential relationships among thyroid hormone, specific miRNAs, and oxidative stress in liver cancer is available. In this review, we discuss the effects of thyroid hormone on oxidative stress-related miRNAs that potentially have a positive or negative impact on liver cancer. Additionally, supporting evidence from clinical and animal experiments is provided. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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18 pages, 2175 KiB  
Review
Cross-Talk between Mitochondrial Dysfunction-Provoked Oxidative Stress and Aberrant Noncoding RNA Expression in the Pathogenesis and Pathophysiology of SLE
by Chang-Youh Tsai, Song-Chou Hsieh, Cheng-Shiun Lu, Tsai-Hung Wu, Hsien-Tzung Liao, Cheng-Han Wu, Ko-Jen Li, Yu-Min Kuo, Hui-Ting Lee, Chieh-Yu Shen and Chia-Li Yu
Int. J. Mol. Sci. 2019, 20(20), 5183; https://doi.org/10.3390/ijms20205183 - 19 Oct 2019
Cited by 28 | Viewed by 5840
Abstract
Systemic lupus erythematosus (SLE) is a prototype of systemic autoimmune disease involving almost every organ. Polygenic predisposition and complicated epigenetic regulations are the upstream factors to elicit its development. Mitochondrial dysfunction-provoked oxidative stress may also play a crucial role in it. Classical epigenetic [...] Read more.
Systemic lupus erythematosus (SLE) is a prototype of systemic autoimmune disease involving almost every organ. Polygenic predisposition and complicated epigenetic regulations are the upstream factors to elicit its development. Mitochondrial dysfunction-provoked oxidative stress may also play a crucial role in it. Classical epigenetic regulations of gene expression may include DNA methylation/acetylation and histone modification. Recent investigations have revealed that intracellular and extracellular (exosomal) noncoding RNAs (ncRNAs), including microRNAs (miRs), and long noncoding RNAs (lncRNAs), are the key molecules for post-transcriptional regulation of messenger (m)RNA expression. Oxidative and nitrosative stresses originating from mitochondrial dysfunctions could become the pathological biosignatures for increased cell apoptosis/necrosis, nonhyperglycemic metabolic syndrome, multiple neoantigen formation, and immune dysregulation in patients with SLE. Recently, many authors noted that the cross-talk between oxidative stress and ncRNAs can trigger and perpetuate autoimmune reactions in patients with SLE. Intracellular interactions between miR and lncRNAs as well as extracellular exosomal ncRNA communication to and fro between remote cells/tissues via plasma or other body fluids also occur in the body. The urinary exosomal ncRNAs can now represent biosignatures for lupus nephritis. Herein, we’ll briefly review and discuss the cross-talk between excessive oxidative/nitrosative stress induced by mitochondrial dysfunction in tissues/cells and ncRNAs, as well as the prospect of antioxidant therapy in patients with SLE. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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13 pages, 1216 KiB  
Review
MicroRNA and Oxidative Stress Interplay in the Context of Breast Cancer Pathogenesis
by Giulia Cosentino, Ilaria Plantamura, Alessandra Cataldo and Marilena V. Iorio
Int. J. Mol. Sci. 2019, 20(20), 5143; https://doi.org/10.3390/ijms20205143 - 17 Oct 2019
Cited by 27 | Viewed by 5104
Abstract
Oxidative stress is a pathological condition determined by a disturbance in reactive oxygen species (ROS) homeostasis. Depending on the entity of the perturbation, normal cells can either restore equilibrium or activate pathways of cell death. On the contrary, cancer cells exploit this phenomenon [...] Read more.
Oxidative stress is a pathological condition determined by a disturbance in reactive oxygen species (ROS) homeostasis. Depending on the entity of the perturbation, normal cells can either restore equilibrium or activate pathways of cell death. On the contrary, cancer cells exploit this phenomenon to sustain a proliferative and aggressive phenotype. In fact, ROS overproduction or their reduced disposal influence all hallmarks of cancer, from genome instability to cell metabolism, angiogenesis, invasion and metastasis. A persistent state of oxidative stress can even initiate tumorigenesis. MicroRNAs (miRNAs) are small non coding RNAs with regulatory functions, which expression has been extensively proven to be dysregulated in cancer. Intuitively, miRNA transcription and biogenesis are affected by the oxidative status of the cell and, in some instances, they participate in defining it. Indeed, it is widely reported the role of miRNAs in regulating numerous factors involved in the ROS signaling pathways. Given that miRNA function and modulation relies on cell type or tumor, in order to delineate a clearer and more exhaustive picture, in this review we present a comprehensive overview of the literature concerning how miRNAs and ROS signaling interplay affects breast cancer progression. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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20 pages, 752 KiB  
Review
MicroRNA Networks Modulate Oxidative Stress in Cancer
by Yang-Hsiang Lin
Int. J. Mol. Sci. 2019, 20(18), 4497; https://doi.org/10.3390/ijms20184497 - 11 Sep 2019
Cited by 76 | Viewed by 5918
Abstract
Imbalanced regulation of reactive oxygen species (ROS) and antioxidant factors in cells is known as “oxidative stress (OS)”. OS regulates key cellular physiological responses through signal transduction, transcription factors and noncoding RNAs (ncRNAs). Increasing evidence indicates that continued OS can cause chronic inflammation, [...] Read more.
Imbalanced regulation of reactive oxygen species (ROS) and antioxidant factors in cells is known as “oxidative stress (OS)”. OS regulates key cellular physiological responses through signal transduction, transcription factors and noncoding RNAs (ncRNAs). Increasing evidence indicates that continued OS can cause chronic inflammation, which in turn contributes to cardiovascular and neurological diseases and cancer development. MicroRNAs (miRNAs) are small ncRNAs that produce functional 18-25-nucleotide RNA molecules that play critical roles in the regulation of target gene expression by binding to complementary regions of the mRNA and regulating mRNA degradation or inhibiting translation. Furthermore, miRNAs function as either tumor suppressors or oncogenes in cancer. Dysregulated miRNAs reportedly modulate cancer hallmarks such as metastasis, angiogenesis, apoptosis and tumor growth. Notably, miRNAs are involved in ROS production or ROS-mediated function. Accordingly, investigating the interaction between ROS and miRNAs has become an important endeavor that is expected to aid in the development of effective treatment/prevention strategies for cancer. This review provides a summary of the essential properties and functional roles of known miRNAs associated with OS in cancers. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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12 pages, 443 KiB  
Review
Development and Clinical Trials of Nucleic Acid Medicines for Pancreatic Cancer Treatment
by Keiko Yamakawa, Yuko Nakano-Narusawa, Nozomi Hashimoto, Masanao Yokohira and Yoko Matsuda
Int. J. Mol. Sci. 2019, 20(17), 4224; https://doi.org/10.3390/ijms20174224 - 29 Aug 2019
Cited by 35 | Viewed by 5154
Abstract
Approximately 30% of pancreatic cancer patients harbor targetable mutations. However, there has been no therapy targeting these molecules clinically. Nucleic acid medicines show high specificity and can target RNAs. Nucleic acid medicine is expected to be the next-generation treatment next to small molecules [...] Read more.
Approximately 30% of pancreatic cancer patients harbor targetable mutations. However, there has been no therapy targeting these molecules clinically. Nucleic acid medicines show high specificity and can target RNAs. Nucleic acid medicine is expected to be the next-generation treatment next to small molecules and antibodies. There are several kinds of nucleic acid drugs, including antisense oligonucleotides, small interfering RNAs, microRNAs, aptamers, decoys, and CpG oligodeoxynucleotides. In this review, we provide an update on current research of nucleic acid-based therapies. Despite the challenging obstacles, we hope that nucleic acid drugs will have a significant impact on the treatment of pancreatic cancer. The combination of genetic diagnosis using next generation sequencing and targeted therapy may provide effective precision medicine for pancreatic cancer patients. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
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