Lyco Lycopene
Description: <b>Lycopene</b> is a naturally occurring carotenoid found predominantly in tomatoes and other red fruits and vegetables. <br>
<br>
Antioxidant Properties:<br>
-Lycopene is a powerful antioxidant. It helps neutralize free radicals, which can reduce oxidative stress—a factor implicated in cancer development. Possible
<a href="https://nestronics.ca/dbx/tbResEdit.php?rid=3273">concern</a>
about interfering with chemotherapy and radiation therapy.
However this
<a href="https://nestronics.ca/dbx/tbResEdit.php?rid=3281">review </a>disagrees.<br>
Inflammation Reduction:<br>
-Some studies suggest that lycopene may help lower levels of inflammation, another process linked to cancer progression<br>
<br>
At supraphysiological or extremely high concentrations, lycopene may have the potential to switch from an antioxidant to a prooxidant role<br>
-The prooxidant effect of lycopene has been observed under conditions of high oxygen tension. In vitro studies have suggested that in environments with elevated oxygen levels, lycopene might promote rather than neutralize the production of reactive oxygen species (ROS).<br>
-The presence of metal ions (such as iron or copper) in the environment can catalyze reactions where antioxidants, including lycopene, contribute to oxidative processes. These metals can interact with lycopene, potentially leading to the formation of radicals.<br>
<br>
The mevalonate pathway produces cholesterol and a variety of isoprenoids, which are important for maintaining cell membrane integrity, protein prenylation, and other essential cellular functions.<br>
-One of the primary enzymes in this pathway is HMG-CoA reductase (3-hydroxy-3-methylglutaryl-coenzyme A reductase), which is the target of statin drugs used for lowering cholesterol.
Some studies suggest that lycopene might downregulate the activity of HMG-CoA reductase or other enzymes in the mevalonate pathway. By doing so, lycopene could potentially reduce the synthesis of cholesterol and isoprenoids that are necessary for rapid cell proliferation—an especially relevant aspect in cancer cells.<br>
<br>
Lycopene typically used in a 100mg/day range for cancer (inhibition of the the Melavonate Pathway)<br>
-also has <a href="tbResList.php?qv=119&tsv=10&wNotes=on&exSp=open">antiplatelet </a>aggregation capability.<br>
<br>
-Note <a href="tbResList.php?qv=119&tsv=1109&wNotes=on&exSp=open">half-life</a> 16–20 days.<br>
<a href="tbResList.php?qv=119&tsv=792&wNotes=on&exSp=open">BioAv</a> Heat processing, especially when combined with a small amount of fat, significantly enhances lycopene’s bioaccessibility and absorption. (20% under optimal conditions)
<br>
Pathways:<br>
<!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑-->
- <a href="tbResList.php?qv=119&tsv=275&wNotes=on">ROS</a> usually goes down, but may go up or down depending on dose and environment. Lycopene may also be modified to be a "oxdiative product" which may change the behaviour.<br>
<!--
- ROS↑ related:
<a href="tbResList.php?qv=119&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm),
<a href="tbResList.php?qv=119&tsv=103&wNotes=on">ER Stress↑</a>,
<a href="tbResList.php?qv=119&tsv=459&wNotes=on">UPR↑</a>,
<a href="tbResList.php?qv=119&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=119&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>,
<a href="tbResList.php?qv=119&tsv=77&wNotes=on">Cyt‑c↑</a>,
<a href="tbResList.php?qv=119&wNotes=on&word=Casp">Caspases↑</a>,
<a href="tbResList.php?qv=119&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>,
<a href="tbResList.php?qv=119&tsv=239&wNotes=on">cl-PARP↑</a>,
<a href="tbResList.php?qv=119&wNotes=on&word=HSP">HSP↓</a>,
<a href="tbResList.php?qv=119&wNotes=on&word=Prx">Prx</a>,
<br>
<!--
<!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, -->
<!--
- Lowers AntiOxidant defense in Cancer Cells:
<a href="tbResList.php?qv=119&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>,
<a href="tbResList.php?qv=119&word=Trx&wNotes=on">TrxR↓**</a>,
<a href="tbResList.php?qv=119&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>,
<a href="tbResList.php?qv=119&tsv=137&wNotes=on&word=GSH↓">GSH↓</a>
<a href="tbResList.php?qv=119&tsv=46&wNotes=on">Catalase↓</a>
<a href="tbResList.php?qv=119&tsv=597&wNotes=on">HO1↓</a>
<a href="tbResList.php?qv=119&wNotes=on&word=GPx">GPx↓</a>
<br>
-->
- Raises
<a href="tbResList.php?qv=119&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a>
defense in Normal Cells:
<a href="tbResList.php?qv=119&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>,
<a href="tbResList.php?qv=119&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>,
<a href="tbResList.php?qv=119&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>,
<a href="tbResList.php?qv=119&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>,
<a href="tbResList.php?qv=119&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>,
<br>
<!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, -->
- lowers
<a href="tbResList.php?qv=119&tsv=953&wNotes=on&word=Inflam">Inflammation</a> :
<a href="tbResList.php?qv=119&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>,
<a href="tbResList.php?qv=119&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>,
<a href="tbResList.php?qv=119&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines :
<a href="tbResList.php?qv=119&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>,
<a href="tbResList.php?qv=119&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>,
<a href="tbResList.php?qv=119&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>,
<a href="tbResList.php?qv=119&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>,
<a href="tbResList.php?qv=119&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a>
<br>
<!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓
inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.-->
- inhibit Growth/Metastases :
<!-- <a href="tbResList.php?qv=119&tsv=604&wNotes=on">TumMeta↓</a>, -->
<!-- <a href="tbResList.php?qv=119&tsv=323&wNotes=on">TumCG↓</a>, -->
<a href="tbResList.php?qv=119&tsv=96&wNotes=on">EMT↓</a>,
<a href="tbResList.php?qv=119&tsv=204&wNotes=on">MMPs↓</a>,
<!-- <a href="tbResList.php?qv=119&tsv=201&wNotes=on">MMP2↓</a>, -->
<a href="tbResList.php?qv=119&tsv=203&wNotes=on">MMP9↓</a>,
<!-- <a href="tbResList.php?qv=119&tsv=308&wNotes=on">TIMP2</a>, -->
<a href="tbResList.php?qv=119&tsv=415&wNotes=on">IGF-1↓</a>,
<a href="tbResList.php?qv=119&tsv=428&wNotes=on">uPA↓</a>,
<a href="tbResList.php?qv=119&tsv=334&wNotes=on">VEGF↓</a>,
<a href="tbResList.php?qv=119&tsv=1284&wNotes=on">ROCK1↓</a>,
<a href="tbResList.php?qv=119&tsv=110&wNotes=on">FAK↓</a>,
<a href="tbResList.php?qv=119&tsv=273&wNotes=on">RhoA↓</a>,
<a href="tbResList.php?qv=119&tsv=214&wNotes=on">NF-κB↓</a>,
<!-- <a href="tbResList.php?qv=119&tsv=79&wNotes=on">CXCR4↓</a>, -->
<!-- <a href="tbResList.php?qv=119&tsv=1247&wNotes=on">SDF1↓</a>, -->
<!-- <a href="tbResList.php?qv=119&tsv=304&wNotes=on">TGF-β↓</a>, -->
<!-- <a href="tbResList.php?qv=119&tsv=719&wNotes=on">α-SMA↓</a>, -->
<a href="tbResList.php?qv=119&tsv=105&wNotes=on">ERK↓</a>
<!-- <a href="tbResList.php?qv=119&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis-->
<br>
<!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, -->
- reactivate genes thereby inhibiting cancer cell growth :
<!-- <a href="tbResList.php?qv=119&tsv=140&wNotes=on">HDAC↓</a>, -->
<!-- <a href="tbResList.php?qv=119&wNotes=on&word=DNMT">DNMTs↓</a>, -->
<a href="tbResList.php?qv=119&tsv=108&wNotes=on">EZH2↓</a>,
<a href="tbResList.php?qv=119&tsv=236&wNotes=on">P53↑</a>,
<!-- <a href="tbResList.php?qv=119&wNotes=on&word=HSP">HSP↓</a>, -->
<a href="tbResList.php?qv=119&tsv=506&wNotes=on">Sp proteins↓</a>,
<!-- <a href="tbResList.php?qv=119&wNotes=on&word=TET">TET↑</a> -->
<br>
<!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ -->
- cause Cell cycle arrest :
<a href="tbResList.php?qv=119&tsv=322&wNotes=on">TumCCA↑</a>,
<a href="tbResList.php?qv=119&tsv=73&wNotes=on">cyclin D1↓</a>,
<a href="tbResList.php?qv=119&tsv=378&wNotes=on">cyclin E↓</a>,
<a href="tbResList.php?qv=119&tsv=467&wNotes=on">CDK2↓</a>,
<a href="tbResList.php?qv=119&tsv=894&wNotes=on">CDK4↓</a>,
<!-- <a href="tbResList.php?qv=119&tsv=895&wNotes=on">CDK6↓</a>, -->
<br>
<!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, -->
- inhibits Migration/Invasion :
<a href="tbResList.php?qv=119&tsv=326&wNotes=on">TumCMig↓</a>,
<a href="tbResList.php?qv=119&tsv=324&wNotes=on">TumCI↓</a>,
<a href="tbResList.php?qv=119&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis -->
<a href="tbResList.php?qv=119&tsv=110&wNotes=on">FAK↓</a>,
<a href="tbResList.php?qv=119&tsv=105&wNotes=on">ERK↓</a>,
<a href="tbResList.php?qv=119&tsv=96&wNotes=on">EMT↓</a>,
<!-- <a href="tbResList.php?qv=119&wNotes=on&word=TOP">TOP1↓</a>, -->
<!-- <a href="tbResList.php?qv=119&tsv=657&wNotes=on">TET1</a>, -->
<br>
<!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS -->
<!--
- inhibits
<a href="tbResList.php?qv=119&tsv=129&wNotes=on">glycolysis</a>
/<a href="tbResList.php?qv=119&tsv=947&wNotes=on">Warburg Effect</a> and
<a href="tbResList.php?qv=119&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> :
<a href="tbResList.php?qv=119&tsv=143&wNotes=on">HIF-1α↓</a>,
<a href="tbResList.php?qv=119&tsv=772&wNotes=on">PKM2↓</a>,
<a href="tbResList.php?qv=119&tsv=35&wNotes=on">cMyc↓</a>,
<a href="tbResList.php?qv=119&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>,
<a href="tbResList.php?qv=119&tsv=906&wNotes=on">LDH↓</a>,
<a href="tbResList.php?qv=119&tsv=175&wNotes=on&word=LDH">LDHA↓</a>,
<a href="tbResList.php?qv=119&tsv=773&wNotes=on">HK2↓</a>,
<a href="tbResList.php?qv=119&wNotes=on&word=PFK">PFKs↓</a>,
<a href="tbResList.php?qv=119&wNotes=on&word=PDK">PDKs↓</a>,
<a href="tbResList.php?qv=119&tsv=847&wNotes=on">ECAR↓</a>,
<a href="tbResList.php?qv=119&tsv=230&wNotes=on">OXPHOS↓</a>,
<a href="tbResList.php?qv=119&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=119&tsv=1278&wNotes=on">Glucose↓</a>,
<a href="tbResList.php?qv=119&tsv=623&wNotes=on">GlucoseCon↓</a>
<br>
-->
<!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)-->
- inhibits
<a href="tbResList.php?qv=119&tsv=447&wNotes=on">angiogenesis↓</a> :
<a href="tbResList.php?qv=119&tsv=334&wNotes=on">VEGF↓</a>,
<a href="tbResList.php?qv=119&tsv=143&wNotes=on">HIF-1α↓</a>,
<!-- <a href="tbResList.php?qv=119&wNotes=on&word=NOTCH">Notch↓</a>, -->
<!-- <a href="tbResList.php?qv=119&wNotes=on&word=FGF">FGF↓</a>, -->
<!-- <a href="tbResList.php?qv=119&wNotes=on&word=PDGF">PDGF↓</a>, -->
<!-- <a href="tbResList.php?qv=119&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, -->
<a href="tbResList.php?qv=119&&wNotes=on&word=ITG">Integrins↓</a>,
<br>
<!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, -->
<!--
- inhibits Cancer Stem Cells :
<a href="tbResList.php?qv=119&tsv=795&wNotes=on">CSC↓</a>,
<a href="tbResList.php?qv=119&tsv=524&wNotes=on">CK2↓</a>,
<a href="tbResList.php?qv=119&tsv=141&wNotes=on">Hh↓</a>,
<a href="tbResList.php?qv=119&tsv=434&wNotes=on">GLi↓</a>,
<a href="tbResList.php?qv=119&tsv=124&wNotes=on">GLi1↓</a>,
<a href="tbResList.php?qv=119&tsv=677&wNotes=on">CD133↓</a>,
<a href="tbResList.php?qv=119&tsv=655&wNotes=on">CD24↓</a>,
<a href="tbResList.php?qv=119&tsv=342&wNotes=on">β-catenin↓</a>,
<a href="tbResList.php?qv=119&tsv=357&wNotes=on">n-myc↓</a>,
<a href="tbResList.php?qv=119&tsv=656&wNotes=on">sox2↓</a>,
<a href="tbResList.php?qv=119&wNotes=on&word=NOTCH">Notch2↓</a>,
<a href="tbResList.php?qv=119&tsv=1024&wNotes=on">nestin↓</a>,
<a href="tbResList.php?qv=119&tsv=508&wNotes=on">OCT4↓</a>,
<br>
-->
<!-- OTHERS : -->
- Others: <a href="tbResList.php?qv=119&tsv=252&wNotes=on">PI3K↓</a>,
<a href="tbResList.php?qv=119&tsv=4&wNotes=on">AKT↓</a>,
<a href="tbResList.php?qv=119&wNotes=on&word=JAK">JAK↓</a>,
<a href="tbResList.php?qv=119&wNotes=on&word=STAT">STAT↓</a>,
<a href="tbResList.php?qv=119&tsv=377&wNotes=on">Wnt↓</a>,
<a href="tbResList.php?qv=119&tsv=342&wNotes=on">β-catenin↓</a>,
<a href="tbResList.php?qv=119&tsv=9&wNotes=on">AMPK</a>,
<!-- <a href="tbResList.php?qv=119&tsv=475&wNotes=on">α↓</a>, -->
<a href="tbResList.php?qv=119&tsv=105&wNotes=on">ERK↓</a>,
<!-- <a href="tbResList.php?qv=119&tsv=1014&wNotes=on">5↓</a>, -->
<a href="tbResList.php?qv=119&tsv=168&wNotes=on">JNK</a>,
- <a href="tbResList.php?qv=119&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br>
<!-- SYNERGIES : -->
- Synergies:
<a href="tbResList.php?qv=119&tsv=1106&wNotes=on">chemo-sensitization</a>,
<a href="tbResList.php?qv=119&tsv=1171&wNotes=on">chemoProtective</a>,
<a href="tbResList.php?qv=119&tsv=1107&wNotes=on">RadioSensitizer</a>,
<a href="tbResList.php?qv=119&tsv=1185&wNotes=on">RadioProtective</a>,
<a href="tbResList.php?qv=119&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>,
<a href="tbResList.php?qv=119&tsv=1105&wNotes=on">Neuroprotective</a>,
<a href="tbResList.php?qv=119&tsv=557&wNotes=on">Cognitive</a>,
<a href="tbResList.php?qv=119&tsv=1175&wNotes=on">Renoprotection</a>,
<a href="tbResList.php?qv=119&tsv=1179&wNotes=on">Hepatoprotective</a>,
<a href="tbResList.php?&qv=119&tsv=1188&wNotes=on">CardioProtective</a>,
<br>
<br>
<!-- SELECTIVE: -->
- Selectivity:
<a href="tbResList.php?qv=119&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a><br>
<br>
<table border="1" cellspacing="0" cellpadding="4">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer Cells</th>
<th>Normal Cells</th>
<th>Label</th>
<th>Primary Interpretation</th>
<th>Notes</th>
</tr>
<tr>
<td>1</td>
<td>Reactive oxygen species (ROS)</td>
<td>↓ ROS</td>
<td>↓ ROS</td>
<td>Driver</td>
<td>Potent antioxidant activity</td>
<td>Lycopene is a strong singlet-oxygen quencher with antioxidant dominance</td>
</tr>
<tr>
<td>2</td>
<td>IGF-1 / PI3K → AKT signaling</td>
<td>↓ IGF-1 signaling; ↓ AKT</td>
<td>↔ minimal</td>
<td>Secondary</td>
<td>Growth factor signaling attenuation</td>
<td>Reduced IGF-1–driven proliferation is a key cancer-relevant effect</td>
</tr>
<tr>
<td>3</td>
<td>Cell cycle regulation</td>
<td>↑ G0/G1 arrest</td>
<td>↔ spared</td>
<td>Phenotypic</td>
<td>Cytostatic growth control</td>
<td>Cell-cycle effects reflect growth factor modulation</td>
</tr>
<tr>
<td>4</td>
<td>Gap junction communication (connexins)</td>
<td>↑ gap junction signaling</td>
<td>↑ gap junction signaling</td>
<td>Secondary</td>
<td>Normalization of cell–cell communication</td>
<td>Enhanced gap junctions are associated with reduced tumor progression</td>
</tr>
<tr>
<td>5</td>
<td>NF-κB / inflammatory signaling</td>
<td>↓ inflammatory signaling</td>
<td>↓ inflammatory tone</td>
<td>Secondary</td>
<td>Anti-inflammatory environment</td>
<td>Inflammation reduction contributes to chemopreventive effects</td>
</tr>
</table>