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Cancers
Special Issues
Role of Antioxidants in Cancer Therapy
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Role of Antioxidants in Cancer Therapy

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 7446

Special Issue Editor

Prof. Dr. Jack L. Arbiser

E-Mail Website
Guest Editor
Medical Center, School of Medicine, Emory University, Atlanta, NY 30322, USA
Interests: respiration; angiogenesis; glycolysis; mitochondria; Sirt3
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Antioxidants in cancer prevention and therapy rank among the most controversial and misunderstood of all treatments of cancer. Conflicting data exist on whether antioxidants prevent or promote the development of cancer, and whether they help or hinder the response to chemotherapy. In this Special Issue, we will provide a framework for the role of antioxidants. This will involve clarifying what an antioxidant is and the role of timing and context. We believe this issue will be of interest to both basic scientists and clinicians who are treating patients with cancer, and patients who are taking over the counter supplements.

Prof. Jack L. Arbiser
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. Cancers 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 2900 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.

Published Papers (3 papers)

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Research

14 pages, 4075 KiB  
Article
Toll-Like Receptor-4 Antagonist Enhances the Repair of Ultraviolet Radiation-Induced DNA Damage and Augments Anti-Tumor Immune Responses in Mice
by Mohammad Asif Sherwani, Ahmed Abdelgawad, Minh Chung, Saad Ibrahim, Mualla Eraslan, Craig A. Elmets and Nabiha Yusuf
Cancers 2021, 13(21), 5406; https://doi.org/10.3390/cancers13215406 - 28 Oct 2021
Cited by 5 | Viewed by 2008
Abstract
Ultraviolet (UV) irradiation of the skin is related to the development of skin cancer. UVB also causes DNA damage in the form of cyclobutane pyrimidine dimers (CPDs), which can result in stable mutations. Toll-like receptor 4 (TLR4), a component of innate immunity, plays [...] Read more.
Ultraviolet (UV) irradiation of the skin is related to the development of skin cancer. UVB also causes DNA damage in the form of cyclobutane pyrimidine dimers (CPDs), which can result in stable mutations. Toll-like receptor 4 (TLR4), a component of innate immunity, plays a key role in cancer. Previous studies from our laboratory have observed that TLR4 deficiency resulted in the repair of UVB-induced DNA damage, inhibition of UVB-induced immune suppression, and carcinogenesis. In this study, we determined the efficacy of TLR4 antagonist TAK-242 in regulation of UVB-induced DNA damage, inflammation, and tumor development. Our results indicate that TAK-242 treatment increased the expression of xeroderma pigmentosum group A (XPA) mRNA, resulting in the repair of UVB-induced CPDs in skin of SKH-1 mice. Treatment with TAK-242 also inhibited the activation of NLR family pyrin domain containing 3 (NLRP3) in UVB-exposed skin of SKH-1 mice. Cutaneous carcinogenesis was significantly reduced in mice treated with TAK-242 in comparison to vehicle-treated mice. The proinflammatory cytokines IL-1β, IL-6, and TNF-α were also found to be significantly greater in vehicle-treated mice than TAK-242-treated mice. Finally, treatment with TAK-242 augmented anti-tumor immune responses in mice. Our data provide further evidence that activation of the TLR4 pathway promotes the development of UV-induced non-melanoma skin cancer mediated at least in part on its negative effects on DNA damage. Moreover, treatment with the TLR4 inhibitor TAK-242 may be effective for prevention of skin cancer. Full article
(This article belongs to the Special Issue Role of Antioxidants in Cancer Therapy)
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20 pages, 4946 KiB  
Article
Honokiol Prevents Non-Alcoholic Steatohepatitis-Induced Liver Cancer via EGFR Degradation through the Glucocorticoid Receptor—MIG6 Axis
by Keiichiro Okuda, Atsushi Umemura, Shiori Umemura, Seita Kataoka, Hiroyoshi Taketani, Yuya Seko, Taichiro Nishikawa, Kanji Yamaguchi, Michihisa Moriguchi, Yoshihiro Kanbara, Jack L. Arbiser, Toshihide Shima, Takeshi Okanoue, Michael Karin and Yoshito Itoh
Cancers 2021, 13(7), 1515; https://doi.org/10.3390/cancers13071515 - 25 Mar 2021
Cited by 8 | Viewed by 2878
Abstract
Non-alcoholic steatohepatitis (NASH) has become a serious public health problem associated with metabolic syndrome. The mechanisms by which NASH induces hepatocellular carcinoma (HCC) remain unknown. There are no approved drugs for treating NASH or preventing NASH-induced HCC. We used a genetic mouse model [...] Read more.
Non-alcoholic steatohepatitis (NASH) has become a serious public health problem associated with metabolic syndrome. The mechanisms by which NASH induces hepatocellular carcinoma (HCC) remain unknown. There are no approved drugs for treating NASH or preventing NASH-induced HCC. We used a genetic mouse model in which HCC was induced via high-fat diet feeding. This mouse model strongly resembles human NASH-induced HCC. The natural product honokiol (HNK) was tested for its preventative effects against NASH progression to HCC. Then, to clarify the mechanisms underlying HCC development, human HCC cells were treated with HNK. Human clinical specimens were also analyzed to explore this study’s clinical relevance. We found that epidermal growth factor receptor (EGFR) signaling was hyperactivated in the livers of mice with NASH and human HCC specimens. Inhibition of EGFR signaling by HNK drastically attenuated HCC development in the mouse model. Mechanistically, HNK accelerated the nuclear translocation of glucocorticoid receptor (GR) and promoted mitogen-inducible gene 6 (MIG6)/ERBB receptor feedback inhibitor 1 (ERRFI1) expression, leading to EGFR degradation and thereby resulting in robust tumor suppression. In human samples, EGFR-positive HCC tissues and their corresponding non-tumor tissues exhibited decreased ERRFI1 mRNA expression. Additionally, GR-positive non-tumor liver tissues displayed lower EGFR expression. Livers from patients with advanced NASH exhibited decreased ERRFI1 expression. EGFR degradation or inactivation represents a novel approach for NASH–HCC treatment and prevention, and the GR–MIG6 axis is a newly defined target that can be activated by HNK and related compounds. Full article
(This article belongs to the Special Issue Role of Antioxidants in Cancer Therapy)
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12 pages, 5089 KiB  
Article
Liposome-Imipramine Blue Inhibits Sonic Hedgehog Medulloblastoma In Vivo
by Tobey J. MacDonald, Jingbo Liu, Bing Yu, Anshu Malhotra, Jenny Munson, Jaekeun C. Park, Kenty Wang, Baowei Fei, Ravi Bellamkonda and Jack Arbiser
Cancers 2021, 13(6), 1220; https://doi.org/10.3390/cancers13061220 - 11 Mar 2021
Cited by 8 | Viewed by 2011
Abstract
Sonic hedgehog subtype of medulloblastoma (SHH MB) with metastasis or specific clinical or molecular alteration shas a poor prognosis and current therapy results in long-term cognitive impairment in the majority of survivors. Thus, a great need exists for new targeted therapeutic approaches to [...] Read more.
Sonic hedgehog subtype of medulloblastoma (SHH MB) with metastasis or specific clinical or molecular alteration shas a poor prognosis and current therapy results in long-term cognitive impairment in the majority of survivors. Thus, a great need exists for new targeted therapeutic approaches to more effectively treat SHH MB in children. Imipramine blue (IB), a novel molecule with anti-tumor properties, inhibits the NADPH oxidase (NOX) family of enzymes, which are critical for SHH MB survival and treatment resistance. In this study, IB was encapsulated within a liposome to form a liposomal nanoparticle, Liposome-IB (Lipo-IB). This complex has the ability to cross the blood–brain barrier and be preferentially taken up by tumor cells within the brain. We demonstrated in vitro that Lipo-IB treatment caused a dose-dependent decrease in SHH MB cell viability and migration. Short-term administration of single agent Lipo-IB treatment of SHH MB in vivo significantly inhibited tumor growth, reduced the tumor volume, including a complete tumor response, and improved survival compared to control treated mice, without any observable toxicity. We conclude that Lipo-IB is a potential novel nanoparticle-based therapeutic for the treatment of SHH MB that warrants further preclinical safety and efficacy testing for development towards clinical investigation. Full article
(This article belongs to the Special Issue Role of Antioxidants in Cancer Therapy)
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