Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 19, Pages -Publisher
MDPI
DOI: 10.3390/ijms231911746
Keywords
ROS; REDOX imbalance; carcinogenesis; malignant cells; quercetin; cancer stem cells
Funding
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [NRF-2020R1I1A2066868]
- National Research Foundation of Korea (NRF) - Korea government (MSIT) [2020R1A5A2019413]
- Korea Health Technology RD Project through the Korea Health Industry Development Institute (KHIDI) - Ministry of Health Welfare, Republic of Korea [HF20C0038, HF20C0116]
- National Research Foundation (NRF) of Korea, Republic of Korea [NRF-2020R1C1C1004573]
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Reactive oxygen species (ROS) play a critical role in carcinogenesis by affecting cell proliferation, survival, and apoptosis through genetic mutations, activation of oncogenes, and increased oxidative stress. Quercetin, a plant-derived bioflavonoid, has been found to scavenge ROS and exhibit anti-tumor properties, particularly in solid tumors. The unique feature of cancer cells, having higher levels of ROS, makes them susceptible to quercetin. Targeting ROS metabolism in cancer cells while sparing normal cells could be a promising approach in cancer therapy.
Reactive oxygen species (ROS) induce carcinogenesis by causing genetic mutations, activating oncogenes, and increasing oxidative stress, all of which affect cell proliferation, survival, and apoptosis. When compared to normal cells, cancer cells have higher levels of ROS, and they are responsible for the maintenance of the cancer phenotype; this unique feature in cancer cells may, therefore, be exploited for targeted therapy. Quercetin (QC), a plant-derived bioflavonoid, is known for its ROS scavenging properties and was recently discovered to have various antitumor properties in a variety of solid tumors. Adaptive stress responses may be induced by persistent ROS stress, allowing cancer cells to survive with high levels of ROS while maintaining cellular viability. However, large amounts of ROS make cancer cells extremely susceptible to quercetin, one of the most available dietary flavonoids. Because of the molecular and metabolic distinctions between malignant and normal cells, targeting ROS metabolism might help overcome medication resistance and achieve therapeutic selectivity while having little or no effect on normal cells. The powerful bioactivity and modulatory role of quercetin has prompted extensive research into the chemical, which has identified a number of pathways that potentially work together to prevent cancer, alongside, QC has a great number of evidences to use as a therapeutic agent in cancer stem cells. This current study has broadly demonstrated the function-mechanistic relationship of quercetin and how it regulates ROS generation to kill cancer and cancer stem cells. Here, we have revealed the regulation and production of ROS in normal cells and cancer cells with a certain signaling mechanism. We demonstrated the specific molecular mechanisms of quercetin including MAPK/ERK1/2, p53, JAK/STAT and TRAIL, AMPK alpha 1/ASK1/p38, RAGE/PI3K/AKT/mTOR axis, HMGB1 and NF-kappa B, Nrf2-induced signaling pathways and certain cell cycle arrest in cancer cell death, and how they regulate the specific cancer signaling pathways as long-searched cancer therapeutics.
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