Posters
Academic Level (Author 1)
Medical Student
Academic Level (Author 2)
Faculty
Discipline/Specialty (Author 2)
Medical Education
Discipline Track
Biomedical Science
Abstract
Cancer cells, compared to normal cells, often exhibit higher levels of reactive oxygen species (ROS) compared to normal cells due to various factors. Despite this, research suggests that cancer cells are more vulnerable to oxidative stress. Given the role of oxidative stress in cancer development, several proposed mechanisms detail how ROS can contribute to tumorigenesis. Targeting pathways that increase ROS production could potentially serve as avenues for cancer treatment or prevention. Transcription factors such as Nrf2, along with genes like P53 and HMOX1, are well-documented in the context of cancer manifestation. Administration of agents such as quercetin, lipid membrane-coated silica-carbon (LSC) hybrid nanoparticles, or antioxidants like glutathione reductase (GR) has shown evidence of inducing or reducing ROS in cancer. However, while oxidative stress contributes to cancer manifestation and progression, the use of exogenous antioxidants remains inconclusive with conflicting results reported in multiple publications. Moreover, antioxidant consumption carries its own risks, necessitating further evidence to address potential dangers in cancer therapy. Nevertheless, moderate intake of antioxidants may potentially slow the risk of cancer development or progression.
We systematically reviewed over 30 recent and pertinent studies on reactive oxygen species (ROS) in cancer manifestation and therapy, utilizing diverse online databases including PubMed, Google Scholar, and Web of Science. Our objective was to consolidate crucial findings from recent research, forming a comprehensive framework that encompasses the current understanding of ROS involvement in acute coronary syndrome. It is noteworthy that all statistical analyses cited in the literature were conducted by the respective authors of the individual studies.
Agents targeting ROS production, as well as proteins and transcription factors implicated in ROS regulation, have garnered significant interest for their potential in mitigating diseases exacerbated by oxidative stress. In physiological contexts, Keap1 governs Nrf2 degradation, a key transcription factor. However, under oxidative stress conditions, Nrf2 undergoes nuclear translocation, thereby enhancing the activity of enzymes like glutathione reductase (GR). Quercetin, a flavonoid with potent antioxidant properties, has been shown to modulate cellular redox status by reducing both glutathione (GSH) levels and GR activity. Interestingly, administration of purified recombinant GR can induce a hyper-reductive state within cells, leading to an unintended consequence: the overproduction of ROS as a compensatory response. This paradoxical effect underscores the delicate balance required for effective antioxidant therapies. Furthermore, LSC nanoparticles have emerged as promising candidates in oxidative stress management by disrupting ATP synthesis pathways. These nanoparticles achieve this by promoting the conversion of nicotinamide adenine dinucleotide (NADH) to its oxidized form (NAD), thereby impeding cellular energy production and potentially limiting the availability of reducing equivalents necessary for ROS generation. Research utilizing heme oxygenase 1 (HMOX1) inhibitors like metalloporphyrin compounds tin protoporphyrin IX (SnPP) and zinc protoporphyrin IX (ZnPP) has shown to enhance tumor cell sensitivity to chemotherapies while reducing free iron levels.
Presentation Type
Poster
Recommended Citation
Cisneros, Fernando IV and Zuo, Alex, "Exploring the Role of Reactive Oxygen Species in Redox Cancer Therapy: Unveiling New Avenues for Treatment" (2024). Research Colloquium. 35.
https://scholarworks.utrgv.edu/colloquium/2024/posters/35
Included in
Exploring the Role of Reactive Oxygen Species in Redox Cancer Therapy: Unveiling New Avenues for Treatment
Cancer cells, compared to normal cells, often exhibit higher levels of reactive oxygen species (ROS) compared to normal cells due to various factors. Despite this, research suggests that cancer cells are more vulnerable to oxidative stress. Given the role of oxidative stress in cancer development, several proposed mechanisms detail how ROS can contribute to tumorigenesis. Targeting pathways that increase ROS production could potentially serve as avenues for cancer treatment or prevention. Transcription factors such as Nrf2, along with genes like P53 and HMOX1, are well-documented in the context of cancer manifestation. Administration of agents such as quercetin, lipid membrane-coated silica-carbon (LSC) hybrid nanoparticles, or antioxidants like glutathione reductase (GR) has shown evidence of inducing or reducing ROS in cancer. However, while oxidative stress contributes to cancer manifestation and progression, the use of exogenous antioxidants remains inconclusive with conflicting results reported in multiple publications. Moreover, antioxidant consumption carries its own risks, necessitating further evidence to address potential dangers in cancer therapy. Nevertheless, moderate intake of antioxidants may potentially slow the risk of cancer development or progression.
We systematically reviewed over 30 recent and pertinent studies on reactive oxygen species (ROS) in cancer manifestation and therapy, utilizing diverse online databases including PubMed, Google Scholar, and Web of Science. Our objective was to consolidate crucial findings from recent research, forming a comprehensive framework that encompasses the current understanding of ROS involvement in acute coronary syndrome. It is noteworthy that all statistical analyses cited in the literature were conducted by the respective authors of the individual studies.
Agents targeting ROS production, as well as proteins and transcription factors implicated in ROS regulation, have garnered significant interest for their potential in mitigating diseases exacerbated by oxidative stress. In physiological contexts, Keap1 governs Nrf2 degradation, a key transcription factor. However, under oxidative stress conditions, Nrf2 undergoes nuclear translocation, thereby enhancing the activity of enzymes like glutathione reductase (GR). Quercetin, a flavonoid with potent antioxidant properties, has been shown to modulate cellular redox status by reducing both glutathione (GSH) levels and GR activity. Interestingly, administration of purified recombinant GR can induce a hyper-reductive state within cells, leading to an unintended consequence: the overproduction of ROS as a compensatory response. This paradoxical effect underscores the delicate balance required for effective antioxidant therapies. Furthermore, LSC nanoparticles have emerged as promising candidates in oxidative stress management by disrupting ATP synthesis pathways. These nanoparticles achieve this by promoting the conversion of nicotinamide adenine dinucleotide (NADH) to its oxidized form (NAD), thereby impeding cellular energy production and potentially limiting the availability of reducing equivalents necessary for ROS generation. Research utilizing heme oxygenase 1 (HMOX1) inhibitors like metalloporphyrin compounds tin protoporphyrin IX (SnPP) and zinc protoporphyrin IX (ZnPP) has shown to enhance tumor cell sensitivity to chemotherapies while reducing free iron levels.