The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism
Identifieur interne : 000333 ( Pmc/Checkpoint ); précédent : 000332; suivant : 000334The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism
Auteurs : Marjorie Reyes-Farias [Espagne] ; Catalina Carrasco-Pozo [Australie]Source :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2019.
Abstract
Cancer is a problem with worldwide importance and is the second leading cause of death globally. Cancer cells reprogram their metabolism to support their uncontrolled expansion by increasing biomass (anabolic metabolism—glycolysis) at the expense of their energy (bioenergetics-mitochondrial function) requirements. In this aspect, metabolic reprogramming stands out as a key biological process in understanding the conversion of a normal cell into a neoplastic precursor. Quercetin is the major representative of the flavonoid subclass of flavonols. Quercetin is ubiquitously present in fruits and vegetables, being one of the most common dietary flavonols in the western diet. The anti-cancer effects of quercetin include its ability to promote the loss of cell viability, apoptosis and autophagy through the modulation of PI3K/Akt/mTOR, Wnt/β-catenin, and MAPK/ERK1/2 pathways. In this review, we discuss the role of quercetin in cancer metabolism, addressing specifically its ability to target molecular pathways involved in glucose metabolism and mitochondrial function.
Url:
DOI: 10.3390/ijms20133177
PubMed: 31261749
PubMed Central: 6651418
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism</title><author><name sortKey="Reyes Farias, Marjorie" sort="Reyes Farias, Marjorie" uniqKey="Reyes Farias M" first="Marjorie" last="Reyes-Farias">Marjorie Reyes-Farias</name><affiliation wicri:level="2"><nlm:aff id="af1-ijms-20-03177">Department of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, 08916 Barcelona, Spain</nlm:aff><country xml:lang="fr">Espagne</country><wicri:regionArea>Department of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, 08916 Barcelona</wicri:regionArea><placeName><region nuts="2" type="communauté">Catalogne</region></placeName></affiliation></author><author><name sortKey="Carrasco Pozo, Catalina" sort="Carrasco Pozo, Catalina" uniqKey="Carrasco Pozo C" first="Catalina" last="Carrasco-Pozo">Catalina Carrasco-Pozo</name><affiliation wicri:level="1"><nlm:aff id="af2-ijms-20-03177">Discovery Biology, Griffith Institute for Drug Discovery, Griffith University, Nathan, QLD 4111, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Discovery Biology, Griffith Institute for Drug Discovery, Griffith University, Nathan, QLD 4111</wicri:regionArea><wicri:noRegion>QLD 4111</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31261749</idno><idno type="pmc">6651418</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6651418</idno><idno type="RBID">PMC:6651418</idno><idno type="doi">10.3390/ijms20133177</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000A14</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000A14</idno><idno type="wicri:Area/Pmc/Curation">000A14</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000A14</idno><idno type="wicri:Area/Pmc/Checkpoint">000333</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000333</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism</title><author><name sortKey="Reyes Farias, Marjorie" sort="Reyes Farias, Marjorie" uniqKey="Reyes Farias M" first="Marjorie" last="Reyes-Farias">Marjorie Reyes-Farias</name><affiliation wicri:level="2"><nlm:aff id="af1-ijms-20-03177">Department of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, 08916 Barcelona, Spain</nlm:aff><country xml:lang="fr">Espagne</country><wicri:regionArea>Department of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, 08916 Barcelona</wicri:regionArea><placeName><region nuts="2" type="communauté">Catalogne</region></placeName></affiliation></author><author><name sortKey="Carrasco Pozo, Catalina" sort="Carrasco Pozo, Catalina" uniqKey="Carrasco Pozo C" first="Catalina" last="Carrasco-Pozo">Catalina Carrasco-Pozo</name><affiliation wicri:level="1"><nlm:aff id="af2-ijms-20-03177">Discovery Biology, Griffith Institute for Drug Discovery, Griffith University, Nathan, QLD 4111, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Discovery Biology, Griffith Institute for Drug Discovery, Griffith University, Nathan, QLD 4111</wicri:regionArea><wicri:noRegion>QLD 4111</wicri:noRegion></affiliation></author></analytic><series><title level="j">International Journal of Molecular Sciences</title><idno type="eISSN">1422-0067</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Cancer is a problem with worldwide importance and is the second leading cause of death globally. Cancer cells reprogram their metabolism to support their uncontrolled expansion by increasing biomass (anabolic metabolism—glycolysis) at the expense of their energy (bioenergetics-mitochondrial function) requirements. In this aspect, metabolic reprogramming stands out as a key biological process in understanding the conversion of a normal cell into a neoplastic precursor. Quercetin is the major representative of the flavonoid subclass of flavonols. Quercetin is ubiquitously present in fruits and vegetables, being one of the most common dietary flavonols in the western diet. The anti-cancer effects of quercetin include its ability to promote the loss of cell viability, apoptosis and autophagy through the modulation of PI3K/Akt/mTOR, Wnt/β-catenin, and MAPK/ERK1/2 pathways. In this review, we discuss the role of quercetin in cancer metabolism, addressing specifically its ability to target molecular pathways involved in glucose metabolism and mitochondrial function.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Ferlay, J" uniqKey="Ferlay J">J. Ferlay</name></author><author><name sortKey="Colombet, M" uniqKey="Colombet M">M. Colombet</name></author><author><name sortKey="Soerjomataram, I" uniqKey="Soerjomataram I">I. Soerjomataram</name></author><author><name sortKey="Mathers, C" uniqKey="Mathers C">C. Mathers</name></author><author><name sortKey="Parkin, D M" uniqKey="Parkin D">D.M. Parkin</name></author><author><name sortKey="Pineros, M" uniqKey="Pineros M">M. Pineros</name></author><author><name sortKey="Znaor, A" uniqKey="Znaor A">A. Znaor</name></author><author><name sortKey="Bray, F" uniqKey="Bray F">F. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Int J Mol Sci</journal-id><journal-id journal-id-type="iso-abbrev">Int J Mol Sci</journal-id><journal-id journal-id-type="publisher-id">ijms</journal-id><journal-title-group><journal-title>International Journal of Molecular Sciences</journal-title></journal-title-group><issn pub-type="epub">1422-0067</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31261749</article-id><article-id pub-id-type="pmc">6651418</article-id><article-id pub-id-type="doi">10.3390/ijms20133177</article-id><article-id pub-id-type="publisher-id">ijms-20-03177</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Reyes-Farias</surname><given-names>Marjorie</given-names></name><xref ref-type="aff" rid="af1-ijms-20-03177">1</xref></contrib><contrib contrib-type="author"><name><surname>Carrasco-Pozo</surname><given-names>Catalina</given-names></name><xref ref-type="aff" rid="af2-ijms-20-03177">2</xref><xref rid="c1-ijms-20-03177" ref-type="corresp">*</xref></contrib></contrib-group><aff id="af1-ijms-20-03177"><label>1</label>Department of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, 08916 Barcelona, Spain</aff><aff id="af2-ijms-20-03177"><label>2</label>Discovery Biology, Griffith Institute for Drug Discovery, Griffith University, Nathan, QLD 4111, Australia</aff><author-notes><corresp id="c1-ijms-20-03177"><label>*</label>Correspondence: <email>c.carrascopozo@griffith.edu.au</email>; Tel.: +61-737-356-034</corresp></author-notes><pub-date pub-type="epub"><day>28</day><month>6</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>7</month><year>2019</year></pub-date><volume>20</volume><issue>13</issue><elocation-id>3177</elocation-id><history><date date-type="received"><day>13</day><month>5</month><year>2019</year></date><date date-type="accepted"><day>25</day><month>6</month><year>2019</year></date></history><permissions><copyright-statement>© 2019 by the authors.</copyright-statement><copyright-year>2019</copyright-year><license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><p>Cancer is a problem with worldwide importance and is the second leading cause of death globally. Cancer cells reprogram their metabolism to support their uncontrolled expansion by increasing biomass (anabolic metabolism—glycolysis) at the expense of their energy (bioenergetics-mitochondrial function) requirements. In this aspect, metabolic reprogramming stands out as a key biological process in understanding the conversion of a normal cell into a neoplastic precursor. Quercetin is the major representative of the flavonoid subclass of flavonols. Quercetin is ubiquitously present in fruits and vegetables, being one of the most common dietary flavonols in the western diet. The anti-cancer effects of quercetin include its ability to promote the loss of cell viability, apoptosis and autophagy through the modulation of PI3K/Akt/mTOR, Wnt/β-catenin, and MAPK/ERK1/2 pathways. In this review, we discuss the role of quercetin in cancer metabolism, addressing specifically its ability to target molecular pathways involved in glucose metabolism and mitochondrial function.</p></abstract><kwd-group><kwd>quercetin</kwd><kwd>cancer</kwd><kwd>glycolysis</kwd><kwd>mitochondrial function</kwd><kwd>PI3K/Akt pathway</kwd></kwd-group></article-meta></front><floats-group><table-wrap id="ijms-20-03177-t001" orientation="portrait" position="float"><object-id pub-id-type="pii">ijms-20-03177-t001_Table 1</object-id><label>Table 1</label><caption><p>Anti-cancer effects of Quercetin (QUE).</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Model</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">QUE Concentration</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Anti-Cancer Effects</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Reference</th></tr></thead><tbody><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">AGS cell line</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">6.25 to 100 μM</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Reduced cell viability in a concentration-dependent manner; at dose 50 µM inhibited 50% growth. When added to SN-38, it improved the anti-proliferation effect of this compound, and increased apoptosis, acting synergistically with SN-38 in the modulation of GSK-3β/β-catenin signaling.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B76-ijms-20-03177" ref-type="bibr">76</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">BALB/c nude mice injected with AGS cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">20 mg/kg BW</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">QUE alone (three times per week) or in combination with irinotecan (10 mg/kg once per week), promoted a significant reduction of tumor size at day 28, and also reduced tumor VEGF-R and VEGF-A levels, protein levels, and reduced COX-2 gene expression. This combination also decreased the TEM population.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B76-ijms-20-03177" ref-type="bibr">76</xref>]</td></tr><tr><td align="center" valign="middle" rowspan="1" colspan="1">MCF-7 and MDA-MB-231 cell lines</td><td align="center" valign="middle" rowspan="1" colspan="1">0 to 100 μM</td><td align="center" valign="middle" rowspan="1" colspan="1">Decreased viability (IC<sub>50</sub> = 30 μM), increased autophagy, suppressed migration rate and reduced MMP-2, MMP-9 and VEGF protein levels. Also, suppressed glucose uptake, lactate production, and expression of PKM2, LDHA, and GLUT1. Similarly, QUE suppressed activation of AKT, mTOR, and p70-S6K. </td><td align="center" valign="middle" rowspan="1" colspan="1">[<xref rid="B64-ijms-20-03177" ref-type="bibr">64</xref>]</td></tr><tr><td align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Mice injected with MCF-7 cells</td><td align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">50 mg/kg BW</td><td align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Inhibited tumor metastasis and progression of breast cancer. It also decreased VEGF, PKM2, and p-AKT levels in tumor tissue.</td><td align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B64-ijms-20-03177" ref-type="bibr">64</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">PC3 cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">1.78 to 100 μM</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inhibited survival in a dose- and time-dependent manner. At a concentration of 40 μM, QUE increased Cyt c, casp 3, casp 8, Bax, Bcl-2, p21<sub>Cip1</sub>, p27<sub>Kip1</sub>, and p53. QUE improved apoptotic effect of MKsi, increased casp 3 and decreased Survivin gene expression. QUE promoted the arrest in the G1 phase cells and decreased cells in the S-phase.<break></break>QUE decreased the phosphorylation of PI3K, Akt, and ERK1/2. QUE decreased p38, NFκB, and Survivin protein levels and increased the PTEN expression. Combined with MKsi, QUE had a greater effect over ERK1/2, p38, NFκB, and Survivin.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B77-ijms-20-03177" ref-type="bibr">77</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">B164A5 murine melanoma cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">150 μM at 72 h</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Reduced OCR and ECAR.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B90-ijms-20-03177" ref-type="bibr">90</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">BC3, BCBL1, and BC1 PEL cell lines.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">12 to 100 μM</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">QUE for 24 h reduced cell survival and growth in a dose-dependent manner, without affecting normal B lymphocytes. QUE 50 μM increased apoptosis rate, increasing the G1 cell phase, PARP cleavage, and nuclear fragmentation/condensation. At this concentration, QUE also inhibited mTOR and Akt<sup>ser473</sup> and promoted degradation of β-catenin.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B62-ijms-20-03177" ref-type="bibr">62</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MCF-7, MDA-MB-231, HBL100 and BT549 breast cancer cells, and OVCAR5, TOV112D, OVCAR3, CAOV3 ovarian cancer cells.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">0.6 to 300 μΜ</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Reduced cell proliferation concentration-dependently.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B58-ijms-20-03177" ref-type="bibr">58</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HBL100 cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">50 μΜ for 24 h</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Increased intracellular accumulation of glucose and promoted lactate depletion into the culture media.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B58-ijms-20-03177" ref-type="bibr">58</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MCF-7 cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">300 μΜ for 48 h</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Increased apoptosis by 25%.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B58-ijms-20-03177" ref-type="bibr">58</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HCT-15 and RKO cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">0 to 200µM</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inhibited cell proliferation, viability, and promoted apoptosis in a concentration dependent manner in cancer cells, but not in normal cells.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B61-ijms-20-03177" ref-type="bibr">61</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HCT-15 cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">142.7 µM (IC<sub>50</sub>)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Reduced glucose consumption and lactate production after 4 h incubation. QUE increased sensitization to 5-FU, improving its effects in glucose metabolism inhibition.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B61-ijms-20-03177" ref-type="bibr">61</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">RKO cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">121.9 µM (IC<sub>50</sub>)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">QUE increased sensitization to 5-FU, improving its effects in glucose metabolism inhibition.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B61-ijms-20-03177" ref-type="bibr">61</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">DL mice</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">25 to 75 mg/kg BW</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Decreased cell viability, mRNA expression and activity of LDH-A, in a dose-dependent manner, without generating liver toxicity. QUE downregulated p85a phosphorylation and Akt gene/protein expression and up-regulated mRNA expression of p53.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B91-ijms-20-03177" ref-type="bibr">91</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Ehrlich ascites tumor cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">26.5 µM</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inhibited lactate production by 78% and of Na<sup>+</sup>-K<sup>+</sup>-ATPase by 85%.</td><td align="center" valign="middle" rowspan="1" colspan="1">[<xref rid="B93-ijms-20-03177" ref-type="bibr">93</xref>]</td></tr><tr><td align="center" valign="middle" rowspan="1" colspan="1">Ehrlich ascites tumor cells</td><td align="center" valign="middle" rowspan="1" colspan="1">13.25 to 66.17 µM</td><td align="center" valign="middle" rowspan="1" colspan="1">At a concentration of 26.5 µM, and after 10 min of treatment, QUE caused 50% inhibition in Na<sup>+</sup>-K<sup>+</sup>-ATPase activity. QUE inhibited aerobic glycolysis and oxidative phosphorylation in a concentration-dependent manner.</td><td align="center" valign="middle" style="border-top:solid thin" rowspan="1" colspan="1">[<xref rid="B92-ijms-20-03177" ref-type="bibr">92</xref>,<xref rid="B126-ijms-20-03177" ref-type="bibr">126</xref>]</td></tr><tr><td align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Ascites tumor cells</td><td align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">33.09 µM</td><td align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Inhibited glycolysis and protein synthesis.</td><td align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B94-ijms-20-03177" ref-type="bibr">94</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Rat thymocytes</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">25 µM</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Prevented glucose uptake induced by mitogenic stimulus.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B127-ijms-20-03177" ref-type="bibr">127</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Ascites tumor cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">0.1µg/mg protein</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inhibited lactate efflux by 50%, increasing internal lactate concentration and decreasing intracellular pH.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B128-ijms-20-03177" ref-type="bibr">128</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HL60 cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">5 to 40 μM</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">QUE, and in combination with 2-DG, induced caspase-dependent late apoptosis, decrease of mitochondrial membrane potential and induction of mIMP, and attenuated Akt and rpS6 phosphorylation. Co-treatment with PI3K/Akt phosphorylation inhibitors increases the apoptosis rate at low concentrations of QUE (10μM) and 2-DG (2 mM).</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B103-ijms-20-03177" ref-type="bibr">103</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Recombinant human PKM2 enzyme</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">9.24 µM</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inhibited PKM2 activity by 50%.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B100-ijms-20-03177" ref-type="bibr">100</xref>]</td></tr></tbody></table></table-wrap><table-wrap id="ijms-20-03177-t002" orientation="portrait" position="float"><object-id pub-id-type="pii">ijms-20-03177-t002_Table 2</object-id><label>Table 2</label><caption><p>Clinical trials evaluating the anti-cancer effect of QUE.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Clinical Study Title</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Description</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Dose, Via and Frequency of Administration</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Benefits</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Limitations</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Ref</th></tr></thead><tbody><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Sulindac and plant compounds in preventing colon cancer</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Study the effectiveness of QUE among other compounds in preventing colon cancer.<break></break>Estimated enrollment: Not specified<break></break>Allocation: Randomized<break></break>Primary Purpose: Prevention</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Orally administered.<break></break>1 of 3 doses twice daily.<break></break>For 6–10 weeks.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Determination of the lowest effective dose of QUE in modulating biomarkers of colon epithelial cell turnover, as an indication of colon cancer prevention.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">No results published, although study completion date was 2006.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B113-ijms-20-03177" ref-type="bibr">113</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pilot study evaluating broccoli sprouts in advanced pancreatic cancer</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Administration of freeze-dried broccoli sprouts rich in QUE and sulforaphane in patients with advanced pancreatic ductal adenocarcinoma<break></break>Estimated enrollment: 40 participants<break></break>Allocation: Randomized<break></break>Intervention Model: Parallel assignment</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Orally administered.<break></break>Capsules with broccoli sprout grain (90 mg sulforaphane daily + QUE-dose not specified).<break></break>For 12 months.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Evaluation of cancer progress or regress in supplementation with capsules rich in QUE.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">This study only declared sulforaphane concentration, but QUE content in the sprout was not specified.<break></break>No results published, although study completion date was 2015. </td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B114-ijms-20-03177" ref-type="bibr">114</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Dietary Intervention in follicular lymphoma (Phase 2)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Assessment of the ability of grape juice (rich in QUE), among several dietary factors, to induce apoptosis, inhibit cell proliferation and modulate tumor cell infiltrate <italic>in vivo</italic>.<break></break>Estimated enrollment: 45 participants<break></break>Allocation: Non-Randomized<break></break>Intervention Model: Single group assignment</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Orally administered.<break></break>Merlot grape juice 100%, 660 mL /495 mL every second day.<break></break>For 16 weeks.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Determination of apoptosis of tumor cells as parameter of intervention efficacy.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">The QUE content of the juice is unknown.<break></break>The study completion date was 2009, however no results have been published yet. </td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B115-ijms-20-03177" ref-type="bibr">115</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Prostate cancer prevention with QUE and genistein</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Evaluation of the effect of QUE or genistein supplementation, in comparison with placebo, against a PSA (prostate-specific antigen) increase.<break></break>Estimated enrollment: 60 participants<break></break>Allocation: Randomized<break></break>Intervention Model: Crossover assignment</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Orally administered.<break></break>500 mg QUE + vitamin C + folic acid + vitamin B3 daily.<break></break>For 6 months.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Determination of QUE effect in PSA levels</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">This study evaluated a QUE supplement combined with other compounds that could act synergically or impact negatively over QUE effect, inducing side effects.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B116-ijms-20-03177" ref-type="bibr">116</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Effect of QUE on green tea polyphenol uptake in prostate tissue from patients with prostate cancer undergoing surgery (Phase 1)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Evaluation of the ability of QUE to enhance the uptake of green tea polyphenols in the prostate tissue of men taking green tea extract and undergoing radical prostatectomy.<break></break>Evaluation of side effects of QUE in combination with green tea.<break></break>Estimated enrollment: 31 participants<break></break>Allocation: Randomized<break></break>Intervention Model: Parallel assignment<break></break>Primary Purpose: Prevention</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Orally administered.<break></break>Green tea polyphenol + QUE twice daily.<break></break>For 3–6 weeks (before undergoing prostatectomy).</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Determination of epigallocatechin gallate, epicatechin gallate and QUE concentration, and their methylated metabolites in prostate tissue and plasma.<break></break>Determination of the extract and QUE on reducing the enzyme activity and protein and gene expression of catechol-O-methyltransferase (COMT), deoxyribonucleic methyltransferase 1 (DNMT1), and multidrug resistance transport protein 1 (MRP1) in prostate tissue. </td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">The concentration of the extract and QUE used is not indicated.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B123-ijms-20-03177" ref-type="bibr">123</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Quercetin chemoprevention for squamous cell carcinoma in patients with fanconi anemia (FA) (Phase 2)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Efficacy of QUE in reducing buccal squamous cell carcinoma.<break></break>Estimated enrollment: 55 participants<break></break>Intervention Model: Single group assignment<break></break>Primary Purpose: Prevention</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Orally administered.<break></break>Twice daily at an adjusted dose based on weight for a maximum total daily dose of 4000 mg/day.<break></break>For 24 months</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Evaluation of the efficacy of QUE in reducing buccal micronuclei and the need for potentially lethal treatment with chemotherapy and/or radiation therapy. </td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">The primary outcome of this study is the reduction of buccal micronuclei in 45 post-hematopoietic cell transplantation (HCT) patients with FA. This is compared to only 10 patients FA patients without a history of HCT.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B124-ijms-20-03177" ref-type="bibr">124</xref>]</td></tr></tbody></table></table-wrap></floats-group></pmc><affiliations><list><country><li>Australie</li><li>Espagne</li></country><region><li>Catalogne</li></region></list><tree><country name="Espagne"><region name="Catalogne"><name sortKey="Reyes Farias, Marjorie" sort="Reyes Farias, Marjorie" uniqKey="Reyes Farias M" first="Marjorie" last="Reyes-Farias">Marjorie Reyes-Farias</name></region></country><country name="Australie"><noRegion><name sortKey="Carrasco Pozo, Catalina" sort="Carrasco Pozo, Catalina" uniqKey="Carrasco Pozo C" first="Catalina" last="Carrasco-Pozo">Catalina Carrasco-Pozo</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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