Abstract
Pancreatic cancer (PC) is a lethal malignancy cancer, and its mortality rates have been increasing worldwide. Diagnosis of this cancer is complicated, as it does not often present symptoms, and most patients present an irremediable tumor having a 5-year survival rate after diagnosis. Regarding treatment, many concerns have also been raised, as most tumors are found at advanced stages. At present, anticancer compounds-rich foods have been utilized to control PC. Among such bioactive molecules, flavonoid compounds have shown excellent anticancer abilities, such as quercetin, which has been used as an adjunctive or alternative drug to PC treatment by inhibitory or stimulatory biological mechanisms including autophagy, apoptosis, cell growth reduction or inhibition, EMT, oxidative stress, and enhancing sensitivity to chemotherapy agents. The recognition that this natural product has beneficial effects on cancer treatment has boosted the researchers' interest towards more extensive studies to use herbal medicine for anticancer purposes. In addition, due to the expensive cost and high rate of side effects of anticancer drugs, attempts have been made to use quercetin but also other flavonoids for preventing and treating PC. Based on related studies, it has been found that the quercetin compound has significant effect on cancerous cell lines as well as animal models. Therefore, it can be used as a supplementary drug to treat a variety of cancers, particularly pancreatic cancer. This review is aimed at discussing the therapeutic effects of quercetin by targeting the molecular signaling pathway and identifying antigrowth, cell proliferation, antioxidative stress, EMT, induction of apoptotic, and autophagic features.
Highlights
Pancreatic cancer (PC) is an increasingly common cancer of the gastrointestinal tract (GIT), with survival rates less than 5% at 5 years after diagnosis, and about 50% of all patients die over 6 months of diagnosis
Since there is not any review article on this subject based on our searches, we aimed to discuss the therapeutic effects of quercetin against pancreatic cancer cells for the first time
The results showed that silencing of a receptor for advanced glycation end products (RAGE) by RAGE-specific siRNA intensified the autophagy and apoptosis through suppressing PI3K/AKT/mTOR axis in MIA Paca-2 and GMC-resistant cells (MIA Paca-2 GMCR cells)
Summary
Pancreatic cancer (PC) is an increasingly common cancer of the gastrointestinal tract (GIT), with survival rates less than 5% at 5 years after diagnosis, and about 50% of all patients die over 6 months of diagnosis. It has been documented that quercetin offers antifungal, antioxidant, cytotoxic, hepatoprotective, and anticancer activities [12] Both quercetin and its derivatives can prevent cancer-related diseases by regulating cellular signaling pathways. Different research studies have analyzed the probable mechanisms through which quercetin exerts its antitumor effects against pancreatic cancer cells. Since there is not any review article on this subject based on our searches, we aimed to discuss the therapeutic effects of quercetin against pancreatic cancer cells for the first time. With an average 5-year survival rate, PC is estimated to be the second cause of cancer-related deaths by 2030 in the United States [21,22,23]. With the limited success of current standard therapies, the search for new and effective treatment strategies and agents is urgently needed
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
