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The Role of Reactive Oxygen Species Responsive Signaling Pathways and MicroRNAs in Anti-cancer Therapies

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 2021) | Viewed by 17822

Special Issue Editors

Prof. Dr. Ryszard Maciejewski

E-Mail Website
Guest Editor
Department of Human Anatomy, Medical University of Lublin, 20-090 Lublin, Poland
Interests: microRNA; microRNA signature; microRNA expression profile; cancer; tumorigenesis; anti-cancer therapies; anoikis; oxidative stress; hypoxia; antioxidant systems
Dr. Joanna Kozak

E-Mail
Guest Editor
Department of Human Anatomy, Medical University of Lublin, 20-090 Lublin, Poland
Interests: microRNA; microRNA signature; microRNA expression profile; cancer; tumorigenesis; anti-cancer therapies; anoikis; oxidative stress; hypoxia; antioxidant systems

Special Issue Information

Dear Colleagues,

For years, microRNAs have attracted growing attention. The powerful regulatory roles of microRNAs in a broad spectrum of biological processes and carcinogenesis are well documented. MicroRNA signatures in distinct cancer entities allow us to look at these molecules as potential biomarkers of the cancer process. However, less is known about microRNA-controlling mechanisms in anticancer therapies. Most of the drugs and radiotherapy applied in the treatment of cancer cells trigger the accumulation of reactive oxygen species (ROS). Therefore, ROS, which were initially recognized as toxic byproducts of aerobic metabolism and which are effectively removed by antioxidants and antioxidative enzymes, seem to play some role in anticancer therapy. The excessive accumulation of ROS can cause cancer cell apoptosis, resulting in antitumor effects. Moreover, the abnormal accumulation of ROS in cancer cells influences the microRNA expression profile. Unsurprisingly, the crosstalk between microRNAs and ROS seems to be significant in anticancer therapy development. Anticancer drug development and the role of microRNAs in this process are of great importance in further investigation. This Special Issue aims to stimulate comprehensive research on insights into the complexity of this problem.

In this Special Issue, we invite original and review papers exploring the impact of ROS and microRNA-activating cellular signaling pathways on anticancer therapy development. Papers highlighting the importance of oxidative stress and the antioxidant system in anticancer therapy are also welcome.

Prof. Dr. Ryszard Maciejewski, Dr. Joanna Kozak 
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

  • microRNA
  • reactive oxygen species (ROS)
  • microRNA expression profile
  • antioxidant system
  • signaling pathways
  • chemotherapy and radiotherapy
  • oxidative stress
  • cancer
  • anticancer therapy resistance

Published Papers (5 papers)

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Research

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13 pages, 3057 KiB  
Article
The Role of E-Cadherin and microRNA on FAK Inhibitor Response in Malignant Pleural Mesothelioma (MPM)
by Man Lee Yuen, Ling Zhuang, Emma M. Rath, Takun Yu, Ben Johnson, Kadir Harun Sarun, Yiwei Wang, Steven Kao, Anthony Linton, Candice Julie Clarke, Brian C. McCaughan, Ken Takahashi, Kenneth Lee and Yuen Yee Cheng
Int. J. Mol. Sci. 2021, 22(19), 10225; https://doi.org/10.3390/ijms221910225 - 23 Sep 2021
Cited by 5 | Viewed by 2088
Abstract
Malignant pleural mesothelioma (MPM) is an aggressive malignancy with limited effective treatment options. Focal adhesion kinase (FAK) inhibitors have been shown to efficiently suppress MPM cell growth initially, with limited utility in the current clinical setting. In this study, we utilised a large [...] Read more.
Malignant pleural mesothelioma (MPM) is an aggressive malignancy with limited effective treatment options. Focal adhesion kinase (FAK) inhibitors have been shown to efficiently suppress MPM cell growth initially, with limited utility in the current clinical setting. In this study, we utilised a large collection of MPM cell lines and MPM tissue samples to study the role of E-cadherin (CDH1) and microRNA on the efficacy of FAK inhibitors in MPM. The immunohistochemistry (IHC) results showed that the majority of MPM FFPE samples exhibited either the absence of, or very low, E-cadherin protein expression in MPM tissue. We showed that MPM cells with high CDH1 mRNA levels exhibited resistance to the FAK inhibitor PND-1186. In summary, MPM cells that did not express CDH1 mRNA were sensitive to PND-1186, and MPM cells that retained CDH1 mRNA were resistant. A cell cycle analysis showed that PND-1186 induced cell cycle disruption by inducing the G2/M arrest of MPM cells. A protein−protein interaction study showed that EGFR is linked to the FAK pathway, and a target scan of the microRNAs revealed that microRNAs (miR-17, miR221, miR-222, miR137, and miR148) interact with EGFR 3′UTR. Transfection of MPM cells with these microRNAs sensitised the CHD1-expressing FAK-inhibitor-resistant MPM cells to the FAK inhibitor. Full article
(This article belongs to the Special Issue The Role of Reactive Oxygen Species Responsive Signaling Pathways and MicroRNAs in Anti-cancer Therapies)
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15 pages, 3903 KiB  
Article
MiR-7-5p Is Involved in Ferroptosis Signaling and Radioresistance Thru the Generation of ROS in Radioresistant HeLa and SAS Cell Lines
by Kazuo Tomita, Taisuke Nagasawa, Yoshikazu Kuwahara, Seiji Torii, Kento Igarashi, Mehryar Habibi Roudkenar, Amaneh Mohammadi Roushandeh, Akihiro Kurimasa and Tomoaki Sato
Int. J. Mol. Sci. 2021, 22(15), 8300; https://doi.org/10.3390/ijms22158300 - 2 Aug 2021
Cited by 42 | Viewed by 4279
Abstract
In cancer therapy, radioresistance or chemoresistance cells are major problems. We established clinically relevant radioresistant (CRR) cells that can survive over 30 days after 2 Gy/day X-ray exposures. These cells also show resistance to anticancer agents and hydrogen peroxide (H2O2 [...] Read more.
In cancer therapy, radioresistance or chemoresistance cells are major problems. We established clinically relevant radioresistant (CRR) cells that can survive over 30 days after 2 Gy/day X-ray exposures. These cells also show resistance to anticancer agents and hydrogen peroxide (H2O2). We have previously demonstrated that all the CRR cells examined had up-regulated miR-7-5p and after miR-7-5p knockdown, they lost radioresistance. However, the mechanism of losing radioresistance remains to be elucidated. Therefore, we investigated the role of miR-7-5p in radioresistance by knockdown of miR-7-5p using CRR cells. As a result, knockdown of miR-7-5p increased reactive oxygen species (ROS), mitochondrial membrane potential, and intracellular Fe2+ amount. Furthermore, miR-7-5p knockdown results in the down-regulation of the iron storage gene expression such as ferritin, up-regulation of the ferroptosis marker ALOX12 gene expression, and increases of Liperfluo amount. H2O2 treatment after ALOX12 overexpression led to the enhancement of intracellular H2O2 amount and lipid peroxidation. By contrast, miR-7-5p knockdown seemed not to be involved in COX-2 and glycolysis signaling but affected the morphology of CRR cells. These results indicate that miR-7-5p control radioresistance via ROS generation that leads to ferroptosis. Full article
(This article belongs to the Special Issue The Role of Reactive Oxygen Species Responsive Signaling Pathways and MicroRNAs in Anti-cancer Therapies)
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17 pages, 4213 KiB  
Article
lncRNA CASC19 Contributes to Radioresistance of Nasopharyngeal Carcinoma by Promoting Autophagy via AMPK-mTOR Pathway
by Hongxia Liu, Wang Zheng, Qianping Chen, Yuchuan Zhou, Yan Pan, Jianghong Zhang, Yang Bai and Chunlin Shao
Int. J. Mol. Sci. 2021, 22(3), 1407; https://doi.org/10.3390/ijms22031407 - 30 Jan 2021
Cited by 26 | Viewed by 2866
Abstract
Nasopharyngeal carcinoma (NPC) is one of the most frequent head and neck malignant tumors and is majorly treated by radiotherapy. However, radiation resistance remains a serious obstacle to the successful treatment of NPC. The aim of this study was to discover the underlying [...] Read more.
Nasopharyngeal carcinoma (NPC) is one of the most frequent head and neck malignant tumors and is majorly treated by radiotherapy. However, radiation resistance remains a serious obstacle to the successful treatment of NPC. The aim of this study was to discover the underlying mechanism of radioresistance and to elucidate novel genes that may play important roles in the regulation of NPC radiosensitivity. By using RNA-seq analysis of NPC cell line CNE2 and its radioresistant cell line CNE2R, lncRNA CASC19 was screened out as a candidate radioresistance marker. Both in vitro and in vivo data demonstrated that a high expression level of CASC19 was positively correlated with the radioresistance of NPC, and the radiosensitivity of NPC cells was considerably enhanced by knockdown of CASC19. The incidence of autophagy was enhanced in CNE2R in comparison with CNE2 and another NPC cell line HONE1, and silencing autophagy with LC3 siRNA (siLC3) sensitized NPC cells to irradiation. Furthermore, CASC19 siRNA (siCASC19) suppressed cellular autophagy by inhibiting the AMPK/mTOR pathway and promoted apoptosis through the PARP1 pathway. Our results revealed for the first time that lncRNA CASC19 contributed to the radioresistance of NPC by regulating autophagy. In significance, CASC19 might be a potential molecular biomarker and a new therapeutic target in NPC. Full article
(This article belongs to the Special Issue The Role of Reactive Oxygen Species Responsive Signaling Pathways and MicroRNAs in Anti-cancer Therapies)
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Review

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21 pages, 2113 KiB  
Review
Micro RNAs in Regulation of Cellular Redox Homeostasis
by Sylwia Ciesielska, Izabella Slezak-Prochazka, Patryk Bil and Joanna Rzeszowska-Wolny
Int. J. Mol. Sci. 2021, 22(11), 6022; https://doi.org/10.3390/ijms22116022 - 2 Jun 2021
Cited by 22 | Viewed by 3554
Abstract
In living cells Reactive Oxygen Species (ROS) participate in intra- and inter-cellular signaling and all cells contain specific systems that guard redox homeostasis. These systems contain both enzymes which may produce ROS such as NADPH-dependent and other oxidases or nitric oxide synthases, and [...] Read more.
In living cells Reactive Oxygen Species (ROS) participate in intra- and inter-cellular signaling and all cells contain specific systems that guard redox homeostasis. These systems contain both enzymes which may produce ROS such as NADPH-dependent and other oxidases or nitric oxide synthases, and ROS-neutralizing enzymes such as catalase, peroxiredoxins, thioredoxins, thioredoxin reductases, glutathione reductases, and many others. Most of the genes coding for these enzymes contain sequences targeted by micro RNAs (miRNAs), which are components of RNA-induced silencing complexes and play important roles in inhibiting translation of their targeted messenger RNAs (mRNAs). In this review we describe miRNAs that directly target and can influence enzymes responsible for scavenging of ROS and their possible role in cellular redox homeostasis. Regulation of antioxidant enzymes aims to adjust cells to survive in unstable oxidative environments; however, sometimes seemingly paradoxical phenomena appear where oxidative stress induces an increase in the levels of miRNAs which target genes which are supposed to neutralize ROS and therefore would be expected to decrease antioxidant levels. Here we show examples of such cellular behaviors and discuss the possible roles of miRNAs in redox regulatory circuits and further cell responses to stress. Full article
(This article belongs to the Special Issue The Role of Reactive Oxygen Species Responsive Signaling Pathways and MicroRNAs in Anti-cancer Therapies)
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23 pages, 438 KiB  
Review
Inhibition or Reversal of the Epithelial-Mesenchymal Transition in Gastric Cancer: Pharmacological Approaches
by Joanna Kozak, Alicja Forma, Marcin Czeczelewski, Paweł Kozyra, Elżbieta Sitarz, Elżbieta Radzikowska-Büchner, Monika Sitarz and Jacek Baj
Int. J. Mol. Sci. 2021, 22(1), 277; https://doi.org/10.3390/ijms22010277 - 29 Dec 2020
Cited by 25 | Viewed by 4219
Abstract
Epithelial-mesenchymal transition (EMT) constitutes one of the hallmarks of carcinogenesis consisting in the re-differentiation of the epithelial cells into mesenchymal ones changing the cellular phenotype into a malignant one. EMT has been shown to play a role in the malignant transformation and while [...] Read more.
Epithelial-mesenchymal transition (EMT) constitutes one of the hallmarks of carcinogenesis consisting in the re-differentiation of the epithelial cells into mesenchymal ones changing the cellular phenotype into a malignant one. EMT has been shown to play a role in the malignant transformation and while occurring in the tumor microenvironment, it significantly affects the aggressiveness of gastric cancer, among others. Importantly, after EMT occurs, gastric cancer patients are more susceptible to the induction of resistance to various therapeutic agents, worsening the clinical outcome of patients. Therefore, there is an urgent need to search for the newest pharmacological agents targeting EMT to prevent further progression of gastric carcinogenesis and potential metastases. Therapies targeted at EMT might be combined with other currently available treatment modalities, which seems to be an effective strategy to treat gastric cancer patients. In this review, we have summarized recent advances in gastric cancer treatment in terms of targeting EMT specifically, such as the administration of polyphenols, resveratrol, tangeretin, luteolin, genistein, proton pump inhibitors, terpenes, other plant extracts, or inorganic compounds. Full article
(This article belongs to the Special Issue The Role of Reactive Oxygen Species Responsive Signaling Pathways and MicroRNAs in Anti-cancer Therapies)
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