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Cancers
Special Issues
Role of Oxidative Stress in Cancer
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Role of Oxidative Stress in Cancer

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

Deadline for manuscript submissions: closed (30 January 2022) | Viewed by 5755

Special Issue Editor

Prof. Dr. Spencer Gibson

E-Mail Website
Guest Editor
1. CancerCare Manitoba Research Institute, CancerCare Manitoba, Winnipeg, MB, Canada
2. Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, MB, Canada
3. Kipnes Endowed Chair, Department of Oncology, University of Alberta, Edmonton, AB, Canada
Interests: chronic lymphocytic leukemia; cellular environment; cell death; drug resistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

During cancer progression, oxidative stress plays an important role in many biological functions such as cell survival, migration, proliferation and cell death. Our understanding of how oxidative stress affects cancer cells is becoming clearer—specifically, how various functions of reactive oxygen species (ROS) affect these biological functions. In addition, the role of the microenvironment in cancer also involves oxidative stress. This could involve cancer cells affecting their microenvironment through oxidative stress or noncancer cells affecting oxidative stress in cancer cells. Finally, oxidative stress has been targeted for cancer therapies and provides new strategies for avoiding drug resistance in cancer.

This Special Issue will accept high-quality original research and review articles in the area of oxidative stress and cancer. This will provide insights into how cancer cells regulate oxidative stress and how to apply this knowledge to cancer treatment.

Prof. Dr. Spencer Gibson
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 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.

Keywords

  • reactive oxygen species
  • cell survival
  • hypoxia
  • cell death
  • proliferation
  • migration
  • metabolism
  • growth factors
  • microenvironment

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Published Papers (2 papers)

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Research

17 pages, 8048 KiB  
Article
AF8c, a Multi-Kinase Inhibitor Induces Apoptosis by Activating DR5/Nrf2 via ROS in Colorectal Cancer Cells
by Soyeon Jeong, Ahmed K. Farag, Hye Kyeong Yun, Yoon A. Jeong, Dae Yeong Kim, Min Jee Jo, Seong Hye Park, Bo Ram Kim, Jung Lim Kim, Bu Gyeom Kim, Dae-Hee Lee, Eun Joo Roh and Sang Cheul Oh
Cancers 2022, 14(13), 3043; https://doi.org/10.3390/cancers14133043 - 21 Jun 2022
Cited by 2 | Viewed by 2282
Abstract
Our team has previously reported a series of quinazoline-based lapatinib hybrids as potent kinase-targeting anticancer agents. Among them, AF8c showed a relatively safe profile in colorectal cancer (CRC) cells. In this study, we delineate a novel anticancer activity of AF8c in CRC cells. [...] Read more.
Our team has previously reported a series of quinazoline-based lapatinib hybrids as potent kinase-targeting anticancer agents. Among them, AF8c showed a relatively safe profile in colorectal cancer (CRC) cells. In this study, we delineate a novel anticancer activity of AF8c in CRC cells. AF8c mediated p53-dependent apoptosis of CRC cells via the generation of endoplasmic reticulum (ER) stress and reactive oxygen species (ROS), as well as activation of nuclear respiratory factor 2 alpha subunit (Nrf2) and death receptor 5 (DR5), among others. The silencing of DR5 attenuated the expression levels of Nrf2 and partially inhibited AF8c-induced apoptosis. Additionally, upregulation of Nrf2 by AF8c evoked apoptosis through a decrease in antioxidant levels. Treatment of a CRC mice model with AF8c also resulted in the upregulation of DR5, Nrf2, and CHOP proteins, subsequently leading to a significant decrease in tumor burden. In comparison with lapatinib, AF8c showed higher cellular antiproliferative activity at the tested concentrations in CRC cells and synergized TRAIL effects in CRC cells. Overall, our results suggest that AF8c-induced apoptosis may be associated with DR5/Nrf2 activation through ER stress and ROS generation in CRC cells. These findings indicate that AF8c represents a promising polypharmacological molecule for the treatment of human CRC. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in Cancer)
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21 pages, 5668 KiB  
Article
AKF-D52, a Synthetic Phenoxypyrimidine-Urea Derivative, Triggers Extrinsic/Intrinsic Apoptosis and Cytoprotective Autophagy in Human Non-Small Cell Lung Cancer Cells
by Hyo-Sun Gil, Jeong-Hun Lee, Ahmed K. Farag, Ahmed H. E. Hassan, Kyung-Sook Chung, Jung-Hye Choi, Eun-Joo Roh and Kyung-Tae Lee
Cancers 2021, 13(22), 5849; https://doi.org/10.3390/cancers13225849 - 22 Nov 2021
Cited by 8 | Viewed by 2851
Abstract
Previously, we discovered that 1-(3,5-dimethoxyphenyl)-3-(4-(3-methoxyphenoxy)-2-((4-morpholinophenyl)amino)pyrimidin-5-yl)urea (AKF-D52), a synthetic phenoxypyrimidine urea derivative, acts as a growth inhibitor of various cancer cell types. In this study, we elucidated the antiproliferative properties of AFK-D52 and underlying mechanisms in non-small cell lung cancer (NSCLC) cells and an [...] Read more.
Previously, we discovered that 1-(3,5-dimethoxyphenyl)-3-(4-(3-methoxyphenoxy)-2-((4-morpholinophenyl)amino)pyrimidin-5-yl)urea (AKF-D52), a synthetic phenoxypyrimidine urea derivative, acts as a growth inhibitor of various cancer cell types. In this study, we elucidated the antiproliferative properties of AFK-D52 and underlying mechanisms in non-small cell lung cancer (NSCLC) cells and an A549 xenograft animal model. AKF-D52 was found to induce both caspase-dependent and -independent apoptotic cell death. Furthermore, the mitochondrial component of the AKF-D52-induced apoptosis mechanism involves a reduction in mitochondrial membrane potential and regulation in B cell lymphoma-2 family protein expression. Moreover, AKF-D52 activates the extrinsic pathway through up-regulated expression of death receptor 3 and Fas and then the formation of a death-inducing signaling complex. AKF-D52 also induced autophagy by increasing acidic vesicular organelle formation and microtubule-associated protein 1A/1B-light chain 3-II levels and reducing p62 levels. Notably, pretreatment with autophagy inhibitors enhanced AKF-D52-induced cell death, indicating that the induced autophagy is cytoprotective. AKF-D52 treatment also triggered reactive oxygen species (ROS) production in NSCLC cells, whereas the antioxidant α-tocopherol abolished AKF-D52-induced cell death. In a xenograft lung cancer mouse model, AKF-D52 administration attenuated tumor growth by inducing apoptosis and autophagy in tumor tissues. Collectively, our data indicate that AKF-D52-induced ROS production plays a role in mediating apoptosis and cytoprotective autophagy in NSCLC. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in Cancer)
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