ReviewOxidative medicine and cellular longevity2022
Dietary Phytochemicals Targeting Nrf2 to Enhance the Radiosensitivity of Cancer.
Review in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Phytochemicals and REDOX Modulation: Molecular Mechanisms, Clinical Relevance, and Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- The interplay between RNA m6A modification and radiation biology of cancerous and non-cancerous tissues: a narrative review.Cancer biology & medicine · 2025Review
- Impact of dietary ingredients on radioprotection and radiosensitization: a comprehensive review.Annals of medicine · 2024Review
- Fractionated irradiation promotes radioresistance and decreases oxidative stress by increasing Nrf2 of ALDH-positive nasopharyngeal cancer stem cells.Annals of medicine and surgery (2012) · 2024Article
- Phenolic compounds as Nrf2 inhibitors: potential applications in cancer therapy.Cell communication and signaling : CCS · 2023Review
- Molecular Docking Identifies 1,8-Cineole (Eucalyptol) as A Novel PPARγ Agonist That Alleviates Colon Inflammation.International journal of molecular sciences · 2023Article
- The Self-Administered Use of Complementary and Alternative Medicine (CAM) Supplements and Antioxidants in Cancer Therapy and the Critical Role of Nrf-2-A Systematic Review.Antioxidants (Basel, Switzerland) · 2022Review
- The Nrf2 in Obesity: A Friend or Foe?Antioxidants (Basel, Switzerland) · 2022Review
- The Therapeutic Potential of Kaemferol and Other Naturally Occurring Polyphenols Might Be Modulated by Nrf2-ARE Signaling Pathway: Current Status and Future Direction.Molecules (Basel, Switzerland) · 2022Review
- Delicaflavone Represses Lung Cancer Growth by Activating Antitumor Immune Response through N6-Methyladenosine Transferases and Oxidative Stress.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nowadays, cancer has become the second leading cause of death worldwide. Radiotherapy (RT) is the mainstay in management of carcinoma; however, overcoming radioresistance remains a great challenge to successfully treat cancer. Nrf2 is a key transcription factor that is responsible for maintaining cellular redox homeostasis. Activation of Nrf2 signaling pathway could upregulate multifarious antioxidant and detoxifying enzymes, further scavenging excessive reactive oxygen species (ROS). Despite its cytoprotective roles in normal cells, it could also alleviate oxidative stress and DNA damage caused by RT in cancer cells, thus promoting cancer cell survival. Accumulating evidence indicates that overactivation of Nrf2 is associated with radioresistance; therefore, targeting Nrf2 is a promising strategy to enhance radiosensitivity. Dietary phytochemicals coming from natural products are characterized by low cost, low toxicity, and general availability. Numerous phytochemicals are reported to regulate Nrf2 and intensify the killing capability of RT through diverse mechanisms, including promoting oxidative stress, proapoptosis, and proautophagy as well as inhibiting Nrf2-mediated cytoprotective genes expression. This review summarizes recent advances in radiosensitizing effects of dietary phytochemicals by targeting Nrf2 and discusses the underlying mechanisms, including N6-methyladenosine (m6A) modification of Nrf2 mediated by phytochemicals in cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.