9
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Potential mechanisms of quercetin in cancer prevention: focus on cellular and molecular targets

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Over the past few years, the cancer-related disease has had a high mortality rate and incidence worldwide, despite clinical advances in cancer treatment. The drugs used for cancer therapy, have high side effects in addition to the high cost. Subsequently, to reduce these side effects, many studies have suggested the use of natural bioactive compounds. Among these, which have recently attracted the attention of many researchers, quercetin has such properties. Quercetin, a plant flavonoid found in fresh fruits, vegetables and citrus fruits, has anti-cancer properties by inhibiting tumor proliferation, invasion, and tumor metastasis. Several studies have demonstrated the anti-cancer mechanism of quercetin, and these mechanisms are controlled through several signalling pathways within the cancer cell. Pathways involved in this process include apoptotic, p53, NF-κB, MAPK, JAK/STAT, PI3K/AKT, and Wnt/β-catenin pathways. In addition to regulating these pathways, quercetin controls the activity of oncogenic and tumor suppressor ncRNAs. Therefore, in this comprehensive review, we summarized the regulation of these signalling pathways by quercetin. The modulatory role of quercetin in the expression of various miRNAs has also been discussed. Understanding the basic anti-cancer mechanisms of these herbal compounds can help prevent and manage many types of cancer.

          Related collections

          Most cited references199

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Ultrastructural Characterization of the Lower Motor System in a Mouse Model of Krabbe Disease

          Krabbe disease (KD) is a neurodegenerative disorder caused by the lack of β- galactosylceramidase enzymatic activity and by widespread accumulation of the cytotoxic galactosyl-sphingosine in neuronal, myelinating and endothelial cells. Despite the wide use of Twitcher mice as experimental model for KD, the ultrastructure of this model is partial and mainly addressing peripheral nerves. More details are requested to elucidate the basis of the motor defects, which are the first to appear during KD onset. Here we use transmission electron microscopy (TEM) to focus on the alterations produced by KD in the lower motor system at postnatal day 15 (P15), a nearly asymptomatic stage, and in the juvenile P30 mouse. We find mild effects on motorneuron soma, severe ones on sciatic nerves and very severe effects on nerve terminals and neuromuscular junctions at P30, with peripheral damage being already detectable at P15. Finally, we find that the gastrocnemius muscle undergoes atrophy and structural changes that are independent of denervation at P15. Our data further characterize the ultrastructural analysis of the KD mouse model, and support recent theories of a dying-back mechanism for neuronal degeneration, which is independent of demyelination.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Targeting autophagy in cancer

            Autophagy is a mechanism by which cellular material is delivered to lysosomes for degradation, leading to the basal turnover of cell components and providing energy and macromolecular precursors. Autophagy has opposing, context-dependent roles in cancer, and interventions to both stimulate and inhibit autophagy have been proposed as cancer therapies. This has led to the therapeutic targeting of autophagy in cancer to be sometimes viewed as controversial. In this Review, we suggest a way forwards for the effective targeting of autophagy by understanding the context-dependent roles of autophagy and by capitalizing on modern approaches to clinical trial design.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Autophagosome formation: core machinery and adaptations.

              Eukaryotic cells employ autophagy to degrade damaged or obsolete organelles and proteins. Central to this process is the formation of autophagosomes, double-membrane vesicles responsible for delivering cytoplasmic material to lysosomes. In the past decade many autophagy-related genes, ATG, have been identified that are required for selective and/or nonselective autophagic functions. In all types of autophagy, a core molecular machinery has a critical role in forming sequestering vesicles, the autophagosome, which is the hallmark morphological feature of this dynamic process. Additional components allow autophagy to adapt to the changing needs of the cell.
                Bookmark

                Author and article information

                Contributors
                parina.asgharian@gmail.com
                abbaspirpour94@gmail.com
                kamran_hosseini2015@yahoo.com
                hforouha@gmail.com
                Tohidgasemnejad@gmail.com
                maryam.ranjbar14@yahoo.com
                muzaffarhassan88@gmail.com
                manojkumarpuniya114@gmail.com
                minaei.sohrab@yahoo.com
                t.tarhriz@yahoo.com
                saeedeh.razi@gmail.com
                erasl2006@mail.ru
                javad.sharifirad@gmail.com
                calinadaniela@gmail.com
                chocs@ha.org.hk
                Journal
                Cancer Cell Int
                Cancer Cell Int
                Cancer Cell International
                BioMed Central (London )
                1475-2867
                15 August 2022
                15 August 2022
                2022
                : 22
                : 257
                Affiliations
                [1 ]GRID grid.412888.f, ISNI 0000 0001 2174 8913, Drug Applied Research Center, , Tabriz University of Medical Sciences, ; Tabriz, Iran
                [2 ]GRID grid.412888.f, ISNI 0000 0001 2174 8913, Department of Pharmacognosy, Faculty of Pharmacy, , Tabriz University of Medical Sciences, ; Tabriz, Iran
                [3 ]GRID grid.412888.f, ISNI 0000 0001 2174 8913, Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, , Tabriz University of Medical Sciences, ; Tabriz, Iran
                [4 ]GRID grid.412571.4, ISNI 0000 0000 8819 4698, Student Research Committee, , Shiraz University of Medical Sciences, ; Shiraz, Iran
                [5 ]GRID grid.412571.4, ISNI 0000 0000 8819 4698, Department of Molecular Medicine, Faculty of Advanced Medical Sciences and Technologies, , Shiraz University of Medical Sciences, ; Shiraz, Iran
                [6 ]GRID grid.412888.f, ISNI 0000 0001 2174 8913, Molecular Medicine Research Center, , Biomedicine Institute, Tabriz University of Medical Sciences, ; Tabriz, Iran
                [7 ]GRID grid.464528.9, ISNI 0000 0004 1755 9492, Agro Produce Processing Division, , ICAR—Central Institute of Agricultural Engineering, ; Bhopal, 462038 India
                [8 ]GRID grid.482244.c, ISNI 0000 0001 2301 0701, Chemical and Biochemical Processing Division, , ICAR—Central Institute for Research on Cotton Technology, ; Mumbai, 400019 India
                [9 ]GRID grid.411746.1, ISNI 0000 0004 4911 7066, Department of Biochemistry, School of Medicine, , Iran University of Medical Sciences, ; Tehran, Iran
                [10 ]GRID grid.412888.f, ISNI 0000 0001 2174 8913, Clinical Research Development Unit of Sina Educational, Research, and Treatment Center, , Tabriz University of Medical Sciences, ; Tabriz, Iran
                [11 ]Scientific Production and Technical Center Zhalyn, А20Х3F6 Almaty, Kazakhstan
                [12 ]GRID grid.442126.7, ISNI 0000 0001 1945 2902, Facultad de Medicina, , Universidad del Azuay, ; 14-008 Cuenca, Ecuador
                [13 ]GRID grid.413055.6, ISNI 0000 0004 0384 6757, Department of Clinical Pharmacy, , University of Medicine and Pharmacy of Craiova, ; 200349 Craiova, Romania
                [14 ]GRID grid.415499.4, ISNI 0000 0004 1771 451X, Department of Clinical Oncology, , Queen Elizabeth Hospital, ; Kowloon, Hong Kong, China
                Article
                2677
                10.1186/s12935-022-02677-w
                9380290
                35971151
                e0504259-5b34-4fff-a2e7-5d8e0e820878
                © The Author(s) 2022

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 20 April 2022
                : 8 August 2022
                Categories
                Review
                Custom metadata
                © The Author(s) 2022

                Oncology & Radiotherapy
                quercetin,malignant tumors,pharmacology,signalling pathways,molecular targets

                Comments

                Comment on this article