tbResList Print — Bor Boron

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Product

Bor Boron
Features: micronutrient
Description: <b>Boron</b> is a trace mineral.<br>
Used in treating yeast infections, improving athletic performance, or preventing osteoporosis.<br>
<br>
Current research suggests that boric acid can modulate intercellular calcium levels—with potential implications for cancer therapy—by:<br>
-Altering calcium channel activity and calcium influx,<br>
-Modifying downstream calcium-dependent signaling, and<br>
-Inducing apoptotic pathways preferentially in cancer cells due to their altered calcium handling dynamics.<br>
Abnormal increases in [Ca²⁺]ᵢ can trigger mitochondrial dysfunction and activate calcium-dependent apoptotic pathways. Boric acid has been observed in some cell culture studies to induce apoptosis in cancer cells.<br>
In normal cells, modest changes in [Ca²⁺]ᵢ induced by boric acid may not reach a threshold that triggers apoptosis or other stress responses. This could lead to a relative sparing of normal cells compared to cancer cells.<br>
<br>
Pathways:<br>
1.Calcium Signaling Pathway<br>
In many cases, boron appears to normalize dysregulated calcium levels in cancer cells, often leading to an increase in calcium levels that can trigger calcium-dependent apoptotic pathways.
2.Apoptotic Pathways (Intrinsic and Extrinsic).<br>
Direction of Modulation:<br>
• Boron compounds may enhance the activation of apoptotic cascades.<br>
• Typically, an increase in intracellular calcium (as noted above) can further lead to mitochondrial dysfunction, cytochrome c release, and subsequent caspase activation, thereby promoting apoptosis.<br>
3.PI3K/AKT/mTOR Pathway<br>
• Some studies indicate that boron-containing compounds can inhibit this pathway.<br>
• Inhibition of PI3K/AKT/mTOR signaling reduces survival signals and can decrease cellular proliferation and growth in tumor cell.<br>
4.MAPK/ERK Pathway <br>
Boron may modulate the MAPK/ERK cascade by either dampening overactive mitogenic signals or altering the stress response.<br>
• This modulation can lead to reduced proliferation signals and may promote cell cycle arrest in cancer cells.<br>
5.NF-κB Signaling Pathway<br>
• Some reports indicate that boron compounds can suppress NF-κB activity.<br>
• This suppression might be achieved indirectly through modulation of upstream signals (such as changes in calcium or the cellular redox status) leading to decreased transcription of pro-survival and pro-inflammatory genes.<br>
6.Wnt/β-Catenin Pathway<br>
• Inhibition of Wnt/β-catenin signaling may interfere with proliferation and the maintenance of cancer stem cell populations.<br>
<br>
ROS:<br>
-ROS induction may be dose related.<br>
-Some studies report that when boron compounds are combined with other treatments (like chemotherapy or radiotherapy), there is a synergistic increase in ROS generation.<br>

Boron’s effects in a cancer context generally lean toward:<br>
• Normalizing dysregulated calcium signaling to push cells toward apoptotic death<br>
• Inhibiting pro-survival pathways such as <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC4712861/">PI3K/AKT/mTOR and NF-κB</a><br>
<br>
(1) is essential for the growth and maintenance of bone;<br>
(2) greatly improves wound healing;<br>
(3) beneficially impacts the body's use of estrogen, testosterone, and vitamin D;<br>
(4) boosts magnesium absorption;<br>
(5) reduces levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor α (TNF-α);<br>
(6) raises levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase;<br>
(7) protects against pesticide-induced oxidative stress and heavy-metal toxicity;<br>
(8) improves the brains electrical activity, cognitive performance, and short-term memory for elders;<br>
(9) influences the formation and activity of key biomolecules, such as S-adenosyl methionine (SAM-e) and nicotinamide adenine dinucleotide (NAD(+));<br>
(10) has demonstrated preventive and therapeutic effects in a number of cancers, such as prostate, cervical, and lung cancers, and multiple and non-Hodgkin's lymphoma; and<br>
(11) may help ameliorate the adverse effects of traditional chemotherapeutic agents.<br>


<br>
-Note <a href="tbResList.php?qv=46&tsv=1109&wNotes=on&exSp=open">half-life</a> 21 hrs average<br>
<a href="tbResList.php?qv=46&tsv=792&wNotes=on&exSp=open">BioAv</a> very high, 85-100%
<br>
Pathways:<br>

<!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑-->
- induce
<a href="tbResList.php?qv=46&tsv=275&wNotes=on">ROS</a> productionin cancer cells, while reducing ROS in normal cells.<br>
- ROS↑ related:
<a href="tbResList.php?qv=46&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm),
<a href="tbResList.php?qv=46&tsv=103&wNotes=on">ER Stress↑</a>,
<a href="tbResList.php?qv=46&tsv=459&wNotes=on">UPR↑</a>,
<a href="tbResList.php?qv=46&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=46&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>,(contrary)
<a href="tbResList.php?qv=46&tsv=77&wNotes=on">Cyt‑c↑</a>,
<a href="tbResList.php?qv=46&wNotes=on&word=Casp">Caspases↑</a>,
<a href="tbResList.php?qv=46&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>,
<a href="tbResList.php?qv=46&tsv=239&wNotes=on">cl-PARP↑</a>,(contrary)
<a href="tbResList.php?qv=46&wNotes=on&word=HSP">HSP↓</a>,
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=Prx">Prx</a>, --><!-- mitochondrial antioxidant enzyme-->

<br>

<!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, -->
- Debateable if Lowers AntiOxidant defense in Cancer Cells:
<a href="tbResList.php?qv=46&tsv=226&wNotes=on&word=NRF2">NRF2↓</a>(most contrary),
<!-- <a href="tbResList.php?qv=46&word=Trx&wNotes=on">TrxR↓**</a>, --><!-- major antioxidant system -->
<a href="tbResList.php?qv=46&tsv=298&wNotes=on&word=SOD">SOD↓</a>(some contrary),
<a href="tbResList.php?qv=46&tsv=137&wNotes=on&word=GSH↓">GSH↓</a>,
<a href="tbResList.php?qv=46&tsv=46&wNotes=on">Catalase↓</a>(some contrary),
<a href="tbResList.php?qv=46&tsv=597&wNotes=on">HO1↓</a>(contrary),
<a href="tbResList.php?qv=46&wNotes=on&word=GPx">GPx↓</a>(some contrary)
<br>

- Raises
<a href="tbResList.php?qv=46&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a>
defense in Normal Cells:
<a href="tbResList.php?qv=46&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>,
<a href="tbResList.php?qv=46&tsv=226&wNotes=on&word=NRF2">NRF2↑</a>,
<a href="tbResList.php?qv=46&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>,
<a href="tbResList.php?qv=46&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>,
<a href="tbResList.php?qv=46&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>,
<!-- genes involved in the oxidative stress-antioxidant defense system PRNP, NQO1, and GCLM -->
<br>

<!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, -->
- lowers
<a href="tbResList.php?qv=46&tsv=953&wNotes=on&word=Inflam">Inflammation</a> :
<a href="tbResList.php?qv=46&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>,
<a href="tbResList.php?qv=46&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=235&wNotes=on&word=p38↓">p38↓</a>, --> Pro-Inflammatory Cytokines :
<a href="tbResList.php?qv=46&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>,
<a href="tbResList.php?qv=46&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>,
<a href="tbResList.php?qv=46&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>,
<a href="tbResList.php?qv=46&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>,
<!-- <a href="tbResList.php?qv=46&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=46&tsv=604&wNotes=on">TumMeta↓</a>,
<a href="tbResList.php?qv=46&tsv=323&wNotes=on">TumCG↓</a>,
<a href="tbResList.php?qv=46&tsv=96&wNotes=on">EMT↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=204&wNotes=on">MMPs↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=201&wNotes=on">MMP2↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=203&wNotes=on">MMP9↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=308&wNotes=on">TIMP2</a>, -->
<a href="tbResList.php?qv=46&tsv=415&wNotes=on">IGF-1↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=428&wNotes=on">uPA↓</a>, -->
<a href="tbResList.php?qv=46&tsv=334&wNotes=on">VEGF↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=1284&wNotes=on">ROCK1↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=110&wNotes=on">FAK↓</a>, -->
<a href="tbResList.php?qv=46&tsv=273&wNotes=on">RhoA↓</a>,
<a href="tbResList.php?qv=46&tsv=214&wNotes=on">NF-κB↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=79&wNotes=on">CXCR4↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=1247&wNotes=on">SDF1↓</a>, -->
<a href="tbResList.php?qv=46&tsv=304&wNotes=on">TGF-β↓</a>,
<a href="tbResList.php?qv=46&tsv=719&wNotes=on">α-SMA↓</a>,
<a href="tbResList.php?qv=46&tsv=105&wNotes=on">ERK↓</a>
<!-- <a href="tbResList.php?qv=46&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=46&tsv=140&wNotes=on">HDAC↓</a>,
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=DNMT">DNMTs↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=108&wNotes=on">EZH2↓</a>, -->
<a href="tbResList.php?qv=46&tsv=236&wNotes=on">P53↑</a>,
<a href="tbResList.php?qv=46&wNotes=on&word=HSP">HSP↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=506&wNotes=on">Sp proteins↓</a>, -->
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=TET">TET↑</a> -->
<br>

<!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ -->
- some indication of Cell cycle arrest :
<a href="tbResList.php?qv=46&tsv=322&wNotes=on">TumCCA↑</a>,
<a href="tbResList.php?qv=46&tsv=73&wNotes=on">cyclin D1↓</a>,
<a href="tbResList.php?qv=46&tsv=378&wNotes=on">cyclin E↓</a>,
<a href="tbResList.php?qv=46&tsv=467&wNotes=on">CDK2↓</a>,
<a href="tbResList.php?qv=46&tsv=894&wNotes=on">CDK4↓</a>,
<a href="tbResList.php?qv=46&tsv=895&wNotes=on">CDK6↓</a>,
<br>

<!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, -->
- inhibits Migration/Invasion :
<a href="tbResList.php?qv=46&tsv=326&wNotes=on">TumCMig↓</a>,
<a href="tbResList.php?qv=46&tsv=324&wNotes=on">TumCI↓</a>,
<a href="tbResList.php?qv=46&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis -->
<!-- <a href="tbResList.php?qv=46&tsv=110&wNotes=on">FAK↓</a>, -->
<a href="tbResList.php?qv=46&tsv=105&wNotes=on">ERK↓</a>,
<a href="tbResList.php?qv=46&tsv=96&wNotes=on">EMT↓</a>,
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=TOP">TOP1↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=657&wNotes=on">TET1</a>, -->
<br>

<!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS -->
- small indication of inhibiting
<a href="tbResList.php?qv=46&tsv=129&wNotes=on">glycolysis</a>
<!-- /<a href="tbResList.php?qv=46&tsv=947&wNotes=on">Warburg Effect</a> and
<a href="tbResList.php?qv=46&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> -->:
<a href="tbResList.php?qv=46&tsv=143&wNotes=on">HIF-1α↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=772&wNotes=on">PKM2↓</a>, -->
<a href="tbResList.php?qv=46&tsv=35&wNotes=on">cMyc↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=906&wNotes=on">LDH↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=773&wNotes=on">HK2↓</a>, -->
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=PFK">PFKs↓</a>, -->
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=PDK">PDKs↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=847&wNotes=on">ECAR↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=230&wNotes=on">OXPHOS↓</a>, -->
<a href="tbResList.php?qv=46&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=46&tsv=1278&wNotes=on">Glucose↓</a>,
<!--<a href="tbResList.php?qv=46&tsv=623&wNotes=on">GlucoseCon↓</a> -->
<br>


<!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)-->
- small indication of inhibiting
<a href="tbResList.php?qv=46&tsv=447&wNotes=on">angiogenesis↓</a> :
<a href="tbResList.php?qv=46&tsv=334&wNotes=on">VEGF↓</a>,
<a href="tbResList.php?qv=46&tsv=143&wNotes=on">HIF-1α↓</a>,
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=NOTCH">Notch↓</a>, -->
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=FGF">FGF↓</a>, -->
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=PDGF">PDGF↓</a>, -->
<a href="tbResList.php?qv=46&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>,
<!--<a href="tbResList.php?qv=46&&wNotes=on&word=ITG">Integrins↓</a>, -->
<br>

<!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, -->
<!--
- inhibits Cancer Stem Cells :
<a href="tbResList.php?qv=46&tsv=795&wNotes=on">CSC↓</a>,
<a href="tbResList.php?qv=46&tsv=524&wNotes=on">CK2↓</a>,
<a href="tbResList.php?qv=46&tsv=141&wNotes=on">Hh↓</a>,
<a href="tbResList.php?qv=46&tsv=434&wNotes=on">GLi↓</a>,
<a href="tbResList.php?qv=46&tsv=124&wNotes=on">GLi1↓</a>,
<a href="tbResList.php?qv=46&tsv=677&wNotes=on">CD133↓</a>,
<a href="tbResList.php?qv=46&tsv=655&wNotes=on">CD24↓</a>,
<a href="tbResList.php?qv=46&tsv=342&wNotes=on">β-catenin↓</a>,
<a href="tbResList.php?qv=46&tsv=357&wNotes=on">n-myc↓</a>,
<a href="tbResList.php?qv=46&tsv=656&wNotes=on">sox2↓</a>,
<a href="tbResList.php?qv=46&wNotes=on&word=NOTCH">Notch2↓</a>,
<a href="tbResList.php?qv=46&tsv=1024&wNotes=on">nestin↓</a>,
<a href="tbResList.php?qv=46&tsv=508&wNotes=on">OCT4↓</a>,
<br> -->

<!-- OTHERS : -->
- Others: <a href="tbResList.php?qv=46&tsv=252&wNotes=on">PI3K↓</a>,
<a href="tbResList.php?qv=46&tsv=4&wNotes=on">AKT↓</a>,
<a href="tbResList.php?qv=46&wNotes=on&word=JAK">JAK↓</a>,
<a href="tbResList.php?qv=46&wNotes=on&word=STAT">STAT↓</a>,
<a href="tbResList.php?qv=46&tsv=377&wNotes=on">Wnt↓</a>,
<a href="tbResList.php?qv=46&tsv=342&wNotes=on">β-catenin↓</a>,
<a href="tbResList.php?qv=46&tsv=9&wNotes=on">AMPK</a>,
<!-- <a href="tbResList.php?qv=46&tsv=475&wNotes=on">α↓</a>, -->
<a href="tbResList.php?qv=46&tsv=105&wNotes=on">ERK↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=1014&wNotes=on">5↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=168&wNotes=on">JNK</a>, -->


- <a href="tbResList.php?qv=46&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br>


<!-- SYNERGIES : -->
- Synergies:
<a href="tbResList.php?qv=46&tsv=1106&wNotes=on">chemo-sensitization</a>,
<a href="tbResList.php?qv=46&tsv=1171&wNotes=on">chemoProtective</a>,
<a href="tbResList.php?qv=46&tsv=1107&wNotes=on">RadioSensitizer</a>,
<a href="tbResList.php?qv=46&tsv=1185&wNotes=on">RadioProtective</a>,
<a href="tbResList.php?qv=46&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>,
<a href="tbResList.php?qv=46&tsv=1105&wNotes=on">Neuroprotective</a>,
<a href="tbResList.php?qv=46&tsv=557&wNotes=on">Cognitive</a>,
<a href="tbResList.php?qv=46&tsv=1175&wNotes=on">Renoprotection</a>,
<a href="tbResList.php?qv=46&tsv=1179&wNotes=on">Hepatoprotective</a>,
<a href="tbResList.php?&qv=46&tsv=1188&wNotes=on">CardioProtective</a>,

<br>
<br>
<!-- SELECTIVE: -->
- Selectivity:
<a href="tbResList.php?qv=46&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a><br>

<br>


Boron Pathways for Cancer vs Normal cells
<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>Hormone / growth factor signaling (IGF-1, steroid modulation)</td>
<td>↓ growth-factor-driven proliferation</td>
<td>↔ optimized endocrine balance</td>
<td>Driver</td>
<td>Systemic growth signal modulation</td>
<td>Boron influences IGF-1, estrogen, and androgen signaling, indirectly reducing proliferative drive in hormone-responsive tumors</td>
</tr>

<tr>
<td>2</td>
<td>Inflammatory signaling (NF-κB / cytokines)</td>
<td>↓ pro-tumor inflammation</td>
<td>↓ inflammatory tone</td>
<td>Driver</td>
<td>Anti-inflammatory environment</td>
<td>Reduced chronic inflammation limits tumor-promoting microenvironmental signals</td>
</tr>

<tr>
<td>3</td>
<td>Cell membrane / signal transduction stability</td>
<td>↓ aberrant signaling responsiveness</td>
<td>↑ membrane and signaling stability</td>
<td>Secondary</td>
<td>Signal fidelity normalization</td>
<td>Boron supports membrane function and receptor signaling fidelity rather than directly inhibiting kinases</td>
</tr>

<tr>
<td>4</td>
<td>Mineral metabolism (Ca²⁺, Mg²⁺, vitamin D interaction)</td>
<td>↔ indirect growth restraint</td>
<td>↑ mineral homeostasis</td>
<td>Secondary</td>
<td>Metabolic support vs dysregulation buffering</td>
<td>Improved mineral balance supports normal cell resilience and systemic metabolic health</td>
</tr>

<tr>
<td>5</td>
<td>Reactive oxygen species (ROS)</td>
<td>↑ ROS (secondary, cancer-biased)</td>
<td>↔ or ↓ ROS (buffered)</td>
<td>Secondary</td>
<td>Metabolic-stress–linked oxidative pressure</td>
<td>ROS increase reflects impaired redox buffering and metabolic stress rather than direct redox chemistry</td>
</tr>

<tr>
<td>6</td>
<td>Glutathione (GSH) homeostasis</td>
<td>↓ GSH availability</td>
<td>↔ maintained</td>
<td>Secondary</td>
<td>Reduced antioxidant capacity</td>
<td>GSH depletion arises from impaired synthesis and NADPH support in cancer cells</td>
</tr>


<tr>
<td>7</td>
<td>Apoptosis</td>
<td>↔ minimal induction</td>
<td>↔ protected</td>
<td>Phenotypic</td>
<td>Non-cytotoxic profile</td>
<td>Boron does not act as a direct apoptotic trigger</td>
</tr>

</table>

<pre>
Distinct from compounds of main Redox Driver
| Compound | ROS ↑ mechanism | Category |
| ------------------- | --------------------------- | ------------------- |
| PEITC | Direct electrophilic stress | Redox driver |
| Selenium (selenite) | Redox cycling | Redox driver |
| Thymoquinone | Quinone cycling | Redox driver |
| **Boron** | Metabolic redox imbalance | **Secondary redox** |

</pre>



Pathway results for Effect on Cancer / Diseased Cells

Redox & Oxidative Stress

Catalase↓, 1,   Catalase↑, 1,   Ferroptosis↑, 3,   GCLC↑, 1,   GPx↑, 1,   GPx4↓, 2,   GSH↓, 4,   HDL↓, 1,   HO-1↑, 1,   MDA↑, 3,   MDA↓, 1,   NADHdeh↓, 1,   NQO1↑, 1,   NRF2↑, 2,   NRF2↓, 1,   OSI↑, 1,   ROS↑, 4,   SAM-e↑, 1,   SAM-e↝, 1,   SOD↓, 1,   SOD↑, 1,   TAC↓, 1,   TBARS↑, 1,   TOS↑, 1,   TOS↓, 1,  

Mitochondria & Bioenergetics

p‑MEK↓, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis

ACSL4↑, 1,   cMyc↓, 1,   Glycolysis↝, 1,   LAT↓, 1,   NAD↓, 1,   NAD↝, 1,   PI3K/Akt↝, 1,   PSMB5↓, 1,   TumCM/A↑, 1,  

Cell Death

p‑Akt↓, 1,   Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 11,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   BID↑, 1,   Casp10∅, 1,   Casp3↑, 5,   Casp3↝, 1,   Casp7↑, 2,   Casp8∅, 1,   Casp8↝, 1,   Casp9↝, 1,   Casp9↑, 1,   DR4∅, 1,   DR5∅, 1,   FADD∅, 1,   Ferroptosis↑, 3,   GADD34↑, 1,   GranA↓, 1,   GranB↓, 1,   MAPK↓, 1,   MAPK↝, 1,   miR-127-5p↑, 2,   NOXA↑, 1,   Perforin↓, 1,   sFasL↑, 1,   TumCD↑, 1,   p‑YAP/TEAD↝, 1,  

Kinase & Signal Transduction

p70S6↓, 1,   TSC2↑, 1,  

Transcription & Epigenetics

miR-21↓, 3,   other↓, 1,   other↑, 1,   other↝, 3,   tumCV↓, 1,  

Protein Folding & ER Stress

ATF6↑, 2,   CHOP↑, 1,   CHOP↓, 1,   eIF2α↑, 1,   p‑eIF2α↑, 1,   ER Stress↝, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   GRP94↑, 1,   HSP70/HSPA5↓, 1,   IRE1∅, 1,   UPR↑, 1,  

Autophagy & Lysosomes

Beclin-1↑, 1,   LAMP2↓, 1,   LC3II↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair

ATM↓, 2,   p‑ATM↑, 1,   BRCA1↑, 1,   BRCA2↑, 1,   DNAdam↑, 1,   P53↑, 1,   P53↓, 1,   p‑P53↑, 1,   PARP↓, 2,  

Cell Cycle & Senescence

CDK4∅, 1,   Cyc↓, 2,   cycD1/CCND1∅, 1,   P21↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

BRAF↝, 1,   BRAF↑, 1,   EMT↓, 1,   p‑ERK⇅, 1,   p‑ERK↓, 1,   HDAC↓, 3,   IGF-1↓, 2,   IGF-1↝, 1,   PTEN↝, 1,   PTEN↓, 1,   PTEN↑, 1,   TumCG↓, 2,  

Migration

Ca+2↓, 5,   CD38↑, 1,   Cdc42↓, 2,   CDH1↑, 2,   COL1A1↓, 3,   E-cadherin↑, 1,   ITGA5↑, 3,   ITGB1↑, 3,   LAMA5↑, 3,   miR-130a↓, 1,   MMP3↓, 1,   MOB1↓, 1,   PCBP1↓, 1,   Rac1↓, 1,   Rho↓, 2,   SA↓, 1,   serineP↓, 1,   Snail↑, 3,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 7,   Vim↓, 3,   Zeb1↑, 3,  

Angiogenesis & Vasculature

angioG↓, 1,   ATF4↑, 2,   EGFR↓, 1,   HIF-1↓, 1,   Hif1a↓, 1,   miR-126↑, 1,   VEGF↓, 2,  

Barriers & Transport

SLC12A5↓, 1,  

Immune & Inflammatory Signaling

GNLY↓, 1,   IFN-γ↓, 1,   IL1↓, 2,   IL10↑, 1,   IL6↓, 2,   PD-1↑, 1,   PD-L1↑, 1,   PSA↓, 4,   TNF-α↓, 3,   TNF-α↝, 1,   VitD↑, 1,  

Protein Aggregation

NLRP3↓, 1,  

Hormonal & Nuclear Receptors

AR↓, 1,   CDK6∅, 1,   DHT↑, 1,  

Drug Metabolism & Resistance

BioAv↑, 2,   ChemoSen↑, 2,   Dose↝, 2,   eff↑, 5,   eff↓, 1,   RadioS↑, 1,   selectivity↑, 3,  

Clinical Biomarkers

AR↓, 1,   BRAF↝, 1,   BRAF↑, 1,   BRCA1↑, 1,   EGFR↓, 1,   GutMicro↑, 1,   IL6↓, 2,   PD-L1↑, 1,   PSA↓, 4,   VitD↑, 1,  

Functional Outcomes

AntiCan↑, 4,   chemoP↑, 1,   ChemoSideEff↓, 1,   OS↑, 1,   radioP↑, 1,   RenoP↑, 1,   Risk↓, 7,   Risk∅, 1,   Risk↑, 1,   TumVol↓, 1,  
Total Targets: 190

Pathway results for Effect on Normal Cells

Redox & Oxidative Stress

antiOx↑, 5,   antiOx↓, 1,   Catalase↑, 4,   GPx↑, 2,   GPx↓, 1,   GSH↑, 4,   HO-1↑, 2,   Keap1↓, 1,   lipid-P↓, 3,   lipid-P↑, 1,   MDA↓, 6,   NRF2↑, 4,   ROS↓, 11,   SAM-e↑, 1,   SOD↑, 7,   TOS↓, 2,  

Metal & Cofactor Biology

IronCh↑, 1,  

Mitochondria & Bioenergetics

ATP↝, 1,   MMP↑, 3,  

Core Metabolism/Glycolysis

ALAT↓, 2,   AMPK↑, 2,   FABP4↓, 1,   FASN↓, 1,   glucose↓, 1,   NAD↝, 1,   PPARγ↓, 1,   SREBP1↓, 1,  

Cell Death

Apoptosis↓, 2,   Casp3↓, 1,   Cyt‑c↓, 1,   iNOS↓, 2,  

Transcription & Epigenetics

other↑, 1,   other↝, 1,  

Protein Folding & ER Stress

CHOP↓, 1,   GRP78/BiP↓, 1,   HSP70/HSPA5↑, 1,  

DNA Damage & Repair

DNAdam↓, 2,   PCNA↓, 1,  

Proliferation, Differentiation & Cell State

CEBPA↓, 1,   FGF↑, 1,   STAT3↓, 2,  

Migration

5LO↓, 1,   Ca+2↝, 1,   Ca+2↓, 1,   Ca+2?, 1,   COL1↑, 1,   MMP2↓, 1,   Sema3A/PlexinA1↑, 1,   serineP↓, 1,   TGF-β↑, 1,   α-SMA↑, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature

angioG↑, 1,   NO↓, 2,   VEGF↑, 1,  

Barriers & Transport

GLUT4↓, 1,  

Immune & Inflammatory Signaling

COX2↓, 2,   CRP↓, 1,   CXCR2↑, 1,   IL10↑, 1,   IL1β↓, 2,   IL6↓, 4,   IL8↓, 1,   Inflam↓, 9,   JAK2↓, 2,   MIP‑1α↓, 1,   NF-kB↓, 5,   PGE2↓, 1,   TNF-α↓, 7,   TNF-α↑, 1,   VitD↑, 4,  

Synaptic & Neurotransmission

AChE↓, 2,   BDNF↝, 1,   BDNF↑, 1,  

Protein Aggregation

Aβ↓, 2,  

Hormonal & Nuclear Receptors

cortisol↑, 1,   DHT↑, 1,   SHBG↓, 1,   testos↑, 2,  

Drug Metabolism & Resistance

BioAv↑, 1,   Dose↑, 3,   Dose↝, 1,   eff↑, 4,   eff↓, 1,   Half-Life↑, 2,   Half-Life↝, 3,   selectivity↑, 1,  

Clinical Biomarkers

ALAT↓, 2,   ALP↓, 2,   AST↓, 2,   BMD↑, 4,   BMPs↑, 1,   Calcium↑, 2,   creat↓, 1,   CRP↓, 1,   hs-CRP↓, 2,   IL6↓, 4,   Mag↑, 2,   VitD↑, 4,  

Functional Outcomes

cardioP↑, 1,   chemoP↑, 1,   chemoPv↑, 1,   ChemoSideEff↓, 1,   cognitive↑, 3,   hepatoP↑, 3,   memory↑, 4,   memory↓, 1,   motorD↑, 1,   motorD↓, 1,   neuroP↑, 4,   PDE4↓, 1,   RenoP↓, 1,   RenoP↑, 1,   Risk↓, 3,   toxicity↓, 6,   Wound Healing↑, 1,  
Total Targets: 116

Research papers

Year Title Authors PMID Link Flag
2025Proteomic insights into the anti-cancer mechanisms of boron-based compounds in prostate cancerSevinc Yanarhttps://www.sciencedirect.com/science/article/abs/pii/S22124292250073450
2025BoronNIHhttps://ods.od.nih.gov/factsheets/Boron-HealthProfessional/?uid=1393ae0afe415s160
2025Effects of Boron on Learning and Behavioral Disorders in Rat Autism Model Induced by Intracerebroventricular Propionic AcidNur Akman Alacabey39397138https://pubmed.ncbi.nlm.nih.gov/39397138/0
2025New and potential boron-containing compounds for treatment of Alzheimer's disease and cancersFerah Comert Onder40600330https://pubmed.ncbi.nlm.nih.gov/40600330/0
2024Boric Acid Affects the Expression of DNA Double-Strand Break Repair Factors in A549 Cells and A549 Cancer Stem Cells: An In Vitro StudyTuğba Semerci SevimliPMC11442501https://pmc.ncbi.nlm.nih.gov/articles/PMC11442501/0
2024The analysis of boric acid effect on epithelial-mesenchymal transition of CD133 + CD117 + lung cancer stem cellsTuğba Semerci SevimliPMC11422429https://pmc.ncbi.nlm.nih.gov/articles/PMC11422429/0
2024Evaluation of Boric Acid Treatment on microRNA-127-5p and Metastasis Genes Orchestration of Breast Cancer Stem CellsTuğba Semerci Sevimli38963646https://pubmed.ncbi.nlm.nih.gov/38963646/0
2024Borax induces ferroptosis of glioblastoma by targeting HSPA5/NRF2/GPx4/GSH pathwaysCengiz TuncerPMC10945083https://pmc.ncbi.nlm.nih.gov/articles/PMC10945083/0
2024Protective Effect of Boric Acid Against Ochratoxin A-Induced Toxic Effects in Human Embryonal Kidney Cells (HEK293): A Study on Cytotoxic, Genotoxic, Oxidative, and Apoptotic EffectsAşkın TekinPMC11750931https://pmc.ncbi.nlm.nih.gov/articles/PMC11750931/0
2024Boron in wound healing: a comprehensive investigation of its diverse mechanismsNasrin Sedighi-PirsaraeiPMC11557333https://pmc.ncbi.nlm.nih.gov/articles/PMC11557333/0
2024The protective effects of selenium and boron on cyclophosphamide-induced hepatic oxidative stress, inflammation, and apoptosis in ratsMustafa CengizPMC11481652https://pmc.ncbi.nlm.nih.gov/articles/PMC11481652/0
2024Boron ReportDr. Gary Gonzalezhttps://www.lifeextension.com/magazine/2003/11/report_boron0
2024Boric Acid and Borax Protect Human Lymphocytes from Oxidative Stress and Genotoxicity Induced by 3-Monochloropropane-1,2-diolHasan TurkezPMC11442522https://pmc.ncbi.nlm.nih.gov/articles/PMC11442522/0
2024In Vitro Effects of Boric Acid on Cell Cycle, Apoptosis, and miRNAs in Medullary Thyroid Cancer CellsOnurcan YıldırımPMC11750916https://pmc.ncbi.nlm.nih.gov/articles/PMC11750916/0
2024Boric Acid Alleviates Lipopolysaccharide-Induced Acute Lung Injury in MiceXiaomin Zhanghttps://link.springer.com/article/10.1007/s12011-024-04240-20
2024Synthesis of DNA-Boron Cluster Composites and Assembly into Functional Nanoparticles with Dual, Anti-EGFR, and Anti-c-MYC Oncogene Silencing ActivityDr. Katarzyna Bednarska-Szczepaniak,https://chemistry-europe.onlinelibrary.wiley.com/doi/10.1002/chem.2023035310
2024Boric Acid (Boron) Attenuates AOM-Induced Colorectal Cancer in Rats by Augmentation of Apoptotic and Antioxidant MechanismsAhmed A J Jabbar37770673https://pubmed.ncbi.nlm.nih.gov/37770673/0
2024Borax affects cellular viability by inducing ER stress in hepatocellular carcinoma cells by targeting SLC12A5Ceyhan HaciogluPMC11114215https://pmc.ncbi.nlm.nih.gov/articles/PMC11114215/0
2024The Potential Role of Boron in the Modulation of Gut Microbiota Composition: An In Vivo Pilot StudyNermin Basak SentürkPMC11510266https://pmc.ncbi.nlm.nih.gov/articles/PMC11510266/0
2024Evaluation of Boric Acid Treatment on microRNA‐127‐5p and Metastasis Genes Orchestration of Breast Cancer Stem CellsTuğba Semerci Sevimlihttps://link.springer.com/article/10.1007/s12011-024-04274-60
2023Enhancement of ferroptosis by boric acid and its potential use as chemosensitizer in anticancer chemotherapyAlessandro Corti36468437https://pubmed.ncbi.nlm.nih.gov/36468437/0
2023Therapeutic Efficacy of Boric Acid Treatment on Brain Tissue and Cognitive Functions in Rats with Experimental Alzheimer’s DiseaseÇağrı ÖzdemirPMC10200114https://pmc.ncbi.nlm.nih.gov/articles/PMC10200114/0
2023Redox Mechanisms Underlying the Cytostatic Effects of Boric Acid on Cancer Cells—An Issue Still OpenGiulia Paties MontagnerPMC10294879https://pmc.ncbi.nlm.nih.gov/articles/PMC10294879/0
2023Boric Acid Alters the Expression of DNA Double Break Repair Genes in MCF-7-Derived Breast Cancer Stem CellsTuğba Semerci Sevimli38087035https://pubmed.ncbi.nlm.nih.gov/38087035/0
2023Borax regulates iron chaperone- and autophagy-mediated ferroptosis pathway in glioblastoma cellsCeyhan Hacioglu36988300https://pubmed.ncbi.nlm.nih.gov/36988300/0
2023Boron Derivatives Inhibit the Proliferation of Breast Cancer Cells and Affect Tumor-Specific T Cell Activity In Vitro by Distinct MechanismsEslam Essam Mohammed36940038https://pubmed.ncbi.nlm.nih.gov/36940038/0
2023Investigation of cytotoxic antiproliferative and antiapoptotic effects of nanosized boron phosphate filled sodium alginate composite on glioblastoma cancer cellsFatma Sayan Poyraz37934369https://pubmed.ncbi.nlm.nih.gov/37934369/0
2023Organoboronic acids/esters as effective drug and prodrug candidates in cancer treatments: challenge and hopeMothana K Al-OmariPMC10351539https://pmc.ncbi.nlm.nih.gov/articles/PMC10351539/0
2023Does Boric Acid Inhibit Cell Proliferation on MCF-7 and MDA-MB-231 Cells in Monolayer and Spheroid Cultures by Using Apoptosis Pathways?Dilek Bayram37572183https://pubmed.ncbi.nlm.nih.gov/37572183/0
2023Boric Acid Alleviates Gastric Ulcer by Regulating Oxidative Stress and Inflammation-Related Multiple Signaling PathwaysAyşe Çakır Gündoğdu37606879https://pubmed.ncbi.nlm.nih.gov/37606879/0
2023Neuroprotective properties of borax against aluminum hydroxide-induced neurotoxicity: Possible role of Nrf-2/BDNF/AChE pathways in fish brainGonca Alakhttps://www.sciencedirect.com/science/article/abs/pii/S00068993230001120
2023Boric Acid Affects Cell Proliferation, Apoptosis, and Oxidative Stress in ALL CellsBüşra Hilal38015327https://pubmed.ncbi.nlm.nih.gov/38015327/0
2023Boric Acid Exhibits Anticancer Properties in Human Endometrial Cancer Ishikawa CellsAyşe Çakır GündoğduPMC10531031https://pmc.ncbi.nlm.nih.gov/articles/PMC10531031/0
2022Boric acid exert anti-cancer effect in poorly differentiated hepatocellular carcinoma cells via inhibition of AKT signaling pathwayErkan Kahraman35868168https://pubmed.ncbi.nlm.nih.gov/35868168/0
2022Cytotoxic and Apoptotic Effects of the Combination of Borax (Sodium Tetraborate) and 5-Fluorouracil on DLD-1 Human Colorectal Adenocarcinoma Cell LineÖmer Faruk KIRLANGIÇPMC9438760https://pmc.ncbi.nlm.nih.gov/articles/PMC9438760/0
2022Calcium fructoborate regulate colon cancer (Caco-2) cytotoxicity through modulation of apoptosisMehmet A Kisacam35174920https://pubmed.ncbi.nlm.nih.gov/35174920/0
2022Mineral requirements for mitochondrial function: A connection to redox balance and cellular differentiationDavid W. Killileahttps://www.sciencedirect.com/science/article/pii/S08915849220007520
2022The Boron Advantage: The Evolution and Diversification of Boron’s Applications in Medicinal ChemistryKatia Messnerhttps://www.mdpi.com/1424-8247/15/3/2640
2022Effect of boron element on photoaging in ratsSeda Gulhttps://www.sciencedirect.com/science/article/abs/pii/S10111344220005490
2022Anti-cancer effect of boron derivatives on small-cell lung cancerEmre Cebeci35007916https://pubmed.ncbi.nlm.nih.gov/35007916/0
2022Boric acid suppresses cell proliferation by TNF signaling pathway mediated apoptosis in SW-480 human colon cancer lineMurat Sevimli35219976https://pubmed.ncbi.nlm.nih.gov/35219976/0
2021Boron Level in the Prostate of the Normal Human: A Systematic ReviewProf. Dr. V. Zaichickhttps://unisciencepub.com/wp-content/uploads/2021/04/Boron-Level-in-the-Prostate-of-the-Normal-Human-A-Systematic-Review.pdf0
2021Investigation of The Apoptotic and Antiproliferative Effects of Boron on CCL-233 Human Colon Cancer CellsŞahabettin Can ÖzyarımPMC8405086https://pmc.ncbi.nlm.nih.gov/articles/PMC8405086/0
2021Boron Intake and decreased risk of mortality in kidney transplant recipientsDaan KremerPMC8854244https://pmc.ncbi.nlm.nih.gov/articles/PMC8854244/0
2021Boric acid as a promising agent in the treatment of ovarian cancer: Molecular mechanismsUmit Cabus34175401https://pubmed.ncbi.nlm.nih.gov/34175401/0
2021Polymers Based on Phenyl Boric Acid in Tumor-Targeted TherapyDexia Luo33438559https://pubmed.ncbi.nlm.nih.gov/33438559/0
2021Plasma boron concentrations in the general population: a cross-sectional analysis of cardio-metabolic and dietary correlatesKatharina S WeberPMC8921125https://pmc.ncbi.nlm.nih.gov/articles/PMC8921125/0
2021Boron Contents of German Mineral and Medicinal Waters and Their Bioavailability in Drosophila melanogaster and HumansUlrike Seidelhttps://onlinelibrary.wiley.com/doi/full/10.1002/mnfr.2021003450
2021Promising potential of boron compounds against Glioblastoma: In Vitro antioxidant, anti-inflammatory and anticancer studiesHasan Turkez34293392https://pubmed.ncbi.nlm.nih.gov/34293392/0
2020Boron Chemistry for Medical ApplicationsFayaz AliPMC7071021https://pmc.ncbi.nlm.nih.gov/articles/PMC7071021/0
2020In vitro effects of boric acid on human liver hepatoma cell line (HepG2) at the half-maximal inhibitory concentrationAysegul Tombulogluhttps://www.sciencedirect.com/science/article/abs/pii/S0946672X203013830
2020The potential role of borophene as a radiosensitizer in boron neutron capture therapy (BNCT) and particle therapy (PT)Pengyuan Qi32342085https://pubmed.ncbi.nlm.nih.gov/32342085/0
2020High Concentrations of Boric Acid Trigger Concentration-Dependent Oxidative Stress, Apoptotic Pathways and Morphological Alterations in DU-145 Human Prostate Cancer Cell LineCeyhan Hacioglu31066018https://pubmed.ncbi.nlm.nih.gov/31066018/0
2020Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid BetaCeyhan Haciogluhttps://link.springer.com/article/10.1007/s12011-020-02511-20
2019Boron inhibits apoptosis in hyperapoptosis condition: Acts by stabilizing the mitochondrial membrane and inhibiting matrix remodelingIndusmita Routrayhttps://www.sciencedirect.com/science/article/abs/pii/S03044165183032090
2019Boron's neurophysiological effects and tumoricidal activity on glioblastoma cells with implications for clinical treatmentMeric A Altinoz30885023https://pubmed.ncbi.nlm.nih.gov/30885023/0
2019BoronForrest H NielsenPMC7442337https://pmc.ncbi.nlm.nih.gov/articles/PMC7442337/0
2018Using Boron Supplementation in Cancer Prevention and Treatment: A Review ArticleSomayeh Nikkhahhttps://www.researchgate.net/publication/352786926_Using_Boron_Supplementation_in_Cancer_Prevention_and_Treatment_A_Review_Article0
2018Discovery of boron-containing compounds as Aβ aggregation inhibitors and antioxidants for the treatment of Alzheimer's diseaseChuan-Jun Luhttps://pmc.ncbi.nlm.nih.gov/articles/PMC6254047/0
2018Boron Affects the Development of the Kidney Through Modulation of Apoptosis, Antioxidant Capacity, and Nrf2 Pathway in the African Ostrich ChicksHaseeb Khaliq29536335https://pubmed.ncbi.nlm.nih.gov/29536335/0
2018Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant StatusKristin E. Yamadahttps://link.springer.com/article/10.1007/s12011-018-1498-40
2018Boron and InflammationJorge D. Flechashttps://restorativemedicine.org/wp-content/uploads/2018/09/FLechas.Boron-and-Inflammation.pdf0
2018The Effect of Boric Acid and Borax on Oxidative Stress, Inflammation, ER Stress and Apoptosis in Cisplatin Toxication and Nephrotoxicity Developing as a Result of ToxicationÖmer Hazman29500724https://pubmed.ncbi.nlm.nih.gov/29500724/0
2018Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant StatuKristin E Yamada30196486https://pubmed.ncbi.nlm.nih.gov/30196486/0
2017Boron Compounds in the Breast Cancer Cells Chemoprevention and ChemotherapyIon Romulus Scoreihttps://ian-faulkner.com/wp-content/uploads/2017/08/boron-cancer-prevention-23268-2.pdf0
2017A new hope for obesity management: Boron inhibits adipogenesis in progenitor cells through the Wnt/β-catenin pathwayAyşegül Doğanhttps://www.sciencedirect.com/science/article/abs/pii/S00260495173002520
2017Effect of Tumor Microenvironment on Selective Uptake of Boric Acid in HepG2 Human Hepatoma CellsYU-CHI BAIhttps://ar.iiarjournals.org/content/37/11/63470
2017High concentrations of boric acid induce autophagy in cancer cell linesRuslan Al-Alihttps://www.biorxiv.org/content/10.1101/193441v1.full.pdf0
2017Boron-Based Inhibitors of the NLRP3 InflammasomeAlex G. Baldwinhttps://www.cell.com/cell-chemical-biology/fulltext/S2451-9456(17)30309-40
2017In vitro and in vivo antitumour effects of phenylboronic acid against mouse mammary adenocarcinoma 4T1 and squamous carcinoma SCCVII cellsMaja MarasovicPMC6010135https://pmc.ncbi.nlm.nih.gov/articles/PMC6010135/0
2016Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron IntakeSarah E KobylewskiPMC5344959https://pmc.ncbi.nlm.nih.gov/articles/PMC5344959/0
2016A Study on the Anticarcinogenic Effects of Calcium FructoborateBurcu Erbaykent Tepedelen28028787https://pubmed.ncbi.nlm.nih.gov/28028787/0
2015Nothing Boring About BoronLara PizzornoPMC4712861https://pmc.ncbi.nlm.nih.gov/articles/PMC4712861/0
2014Cytotoxic and apoptotic effects of boron compounds on leukemia cell lineZerrin CanturkPMC4698272https://pmc.ncbi.nlm.nih.gov/articles/PMC4698272/0
2014Boric acid induces cytoplasmic stress granule formation, eIF2α phosphorylation, and ATF4 in prostate DU-145 cellsKimberly A HendersonPMC4300416https://pmc.ncbi.nlm.nih.gov/articles/PMC4300416/0
2012Dietary Boron and Hormone Replacement Therapy as Risk Factors for Lung Cancer in WomenS MahabirPMC3390773https://pmc.ncbi.nlm.nih.gov/articles/PMC3390773/0
2012Boron containing compounds as protease inhibitorsReem Smoum22519511https://pubmed.ncbi.nlm.nih.gov/22519511/0
2012Sugar-borate esters--potential chemical agents in prostate cancer chemopreventionRomulus Ion Scorei23293883https://pubmed.ncbi.nlm.nih.gov/23293883/0
2011Phenylboronic acid is a more potent inhibitor than boric acid of key signaling networks involved in cancer cell migrationErin M McAuleyPMC3218604https://pmc.ncbi.nlm.nih.gov/articles/PMC3218604/0
2011Prevalence of Prostate Cancer in High Boron-Exposed Population: A Community-Based StudyTalha Müezzinoğluhttps://www.researchgate.net/publication/50832657_Prevalence_of_Prostate_Cancer_in_High_Boron-Exposed_Population_A_Community-Based_Study0
2011Comparative effects of daily and weekly boron supplementation on plasma steroid hormones and proinflammatory cytokinesMohammad Reza Naghii21129941https://pubmed.ncbi.nlm.nih.gov/21129941/0
2011Growing Evidence for Human Health Benefits of BoronForrest H. Nielsen, PhDhttps://journals.sagepub.com/doi/full/10.1177/21565872114076380
2010Boric acid as a protector against paclitaxel genotoxicityHasan Turkez20300661https://pubmed.ncbi.nlm.nih.gov/20300661/0
2010Boron-containing phenoxyacetanilide derivatives as hypoxia-inducible factor (HIF)-1alpha inhibitorsKazuki Shimizu20083404https://pubmed.ncbi.nlm.nih.gov/20083404/0
2010Boron-containing compounds as preventive and chemotherapeutic agents for cancerRomulus I Scorei19912103https://pubmed.ncbi.nlm.nih.gov/19912103/0
2009Boron deprivation decreases liver S-adenosylmethionine and spermidine and increases plasma homocysteine and cysteine in ratsForrest Harold Nielsen19486830https://pubmed.ncbi.nlm.nih.gov/19486830/0
2009Receptor Activated Ca2+ Release Is Inhibited by Boric Acid in Prostate Cancer CellsKimberly HendersonPMC2698284https://pmc.ncbi.nlm.nih.gov/articles/PMC2698284/0
2009Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cellsWade T Barranco18516691https://pubmed.ncbi.nlm.nih.gov/18516691/0
2009Design, Synthesis, and Biological Activity of Boronic Acid-Based Histone Deacetylase InhibitorsNobuaki Suzukihttps://pubs.acs.org/doi/abs/10.1021/jm900125m0
2008Comparative effects of boric acid and calcium fructoborate on breast cancer cellsR Scorei18176783https://pubmed.ncbi.nlm.nih.gov/18176783/0
2008Dietary Boron and Hormone Replacement Therapy as Risk Factors for Lung Cancer in WomenS MahabirPMC3390773https://pmc.ncbi.nlm.nih.gov/articles/PMC3390773/0
2007Boron intake and prostate cancer riskAlejandro Gonzalez17851770https://pubmed.ncbi.nlm.nih.gov/17851770/0
2007Evaluation of ecological and in vitro effects of boron on prostate cancer risk (United States)Wade T Barranco17186423https://pubmed.ncbi.nlm.nih.gov/17186423/0
2007Mechanism of boric acid cytotoxicity in breast cancer cell linesAnu Elegbedehttps://aacrjournals.org/cancerres/article/67/9_Supplement/3384/537484/Mechanism-of-boric-acid-cytotoxicity-in-breast0
2007https://aacrjournals.org/cancerres/article/67/9_Supplement/4220/535557/Boric-acid-induces-apoptosis-in-both-prostate-andStephen Carperhttps://aacrjournals.org/cancerres/article/67/9_Supplement/4220/535557/Boric-acid-induces-apoptosis-in-both-prostate-and0
2007Effects of dietary boron on cervical cytopathology and on micronucleus frequency in exfoliated buccal cellsMehmet Korkmaz17295277https://pubmed.ncbi.nlm.nih.gov/17295277/0
2007Boron as a Medicinal Ingredient in Oral Natural Health ProductsGovernment of Canadahttps://www.canada.ca/en/health-canada/services/drugs-health-products/reports-publications/natural-health-products/boron-medicinal-ingredient-oral-natural-health-products-natural-health-products-directorate-heath-canada-2007.html0
2007Boron and Prostate Cancer a Model for Understanding Boron BiologyCurtis Eckherthttps://link.springer.com/chapter/10.1007/978-1-4020-5382-5_280
2007The Effect of Boron on the UPR in Prostate Cancer Cells is BiphasicKim Hendersonhttps://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.21.5.a124-d0
2006Cellular changes in boric acid-treated DU-145 prostate cancer cellsW T BarrancoPMC3216419https://pmc.ncbi.nlm.nih.gov/articles/PMC3216419/0
2004Boric acid inhibits human prostate cancer cell proliferationWade T Barranco15500945https://pubmed.ncbi.nlm.nih.gov/15500945/0
2004Dietary boron intake and prostate cancer riskYan Cui15010890https://pubmed.ncbi.nlm.nih.gov/15010890/0
2004Boron supplementation inhibits the growth and local expression of IGF-1 in human prostate adenocarcinoma (LNCaP) tumors in nude miceMaria T Gallardo-Williams14713551https://pubmed.ncbi.nlm.nih.gov/14713551/0
2004EVIDENCE THAT BORON DOWN-REGULATES INFLAMMATION THROUGH THE NF-(KAPPA)B PATHWAYDURICK, KATHYhttps://www.ars.usda.gov/research/publications/publication/?seqNo115=1712870
2003Inhibition of the enzymatic activity of prostate-specific antigen by boric acid and 3-nitrophenyl boronic acidMaria T Gallardo-Williams12481254https://pubmed.ncbi.nlm.nih.gov/12481254/0
2003Boron concentrations in selected foods from borate-producing regions in TurkeyAtilla Simsekhttps://scijournals.onlinelibrary.wiley.com/doi/abs/10.1002/jsfa.14080
2001Diadenosine phosphates and S-adenosylmethionine: novel boron binding biomolecules detected by capillary electrophoresisN V Ralston11420139https://pubmed.ncbi.nlm.nih.gov/11420139/0
1998The nutritional and metabolic effects of boron in humans and animalsS Samman10050922https://pubmed.ncbi.nlm.nih.gov/10050922/0
1994Chemical disposition of boron in animals and humansR F MosemanPMC1566637https://pmc.ncbi.nlm.nih.gov/articles/PMC1566637/0