condition found tbRes List
Bor, Boron: Click to Expand ⟱
Features: micronutrient
Boron is a trace mineral.
Used in treating yeast infections, improving athletic performance, or preventing osteoporosis.

Current research suggests that boric acid can modulate intercellular calcium levels—with potential implications for cancer therapy—by:
-Altering calcium channel activity and calcium influx,
-Modifying downstream calcium-dependent signaling, and
-Inducing apoptotic pathways preferentially in cancer cells due to their altered calcium handling dynamics.
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.
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.

Pathways:
1.Calcium Signaling Pathway
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).
Direction of Modulation:
• Boron compounds may enhance the activation of apoptotic cascades.
• 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.
3.PI3K/AKT/mTOR Pathway
• Some studies indicate that boron-containing compounds can inhibit this pathway.
• Inhibition of PI3K/AKT/mTOR signaling reduces survival signals and can decrease cellular proliferation and growth in tumor cell.
4.MAPK/ERK Pathway
Boron may modulate the MAPK/ERK cascade by either dampening overactive mitogenic signals or altering the stress response.
• This modulation can lead to reduced proliferation signals and may promote cell cycle arrest in cancer cells.
5.NF-κB Signaling Pathway
• Some reports indicate that boron compounds can suppress NF-κB activity.
• 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.
6.Wnt/β-Catenin Pathway
• Inhibition of Wnt/β-catenin signaling may interfere with proliferation and the maintenance of cancer stem cell populations.

ROS:
-ROS induction may be dose related.
-Some studies report that when boron compounds are combined with other treatments (like chemotherapy or radiotherapy), there is a synergistic increase in ROS generation.
Boron’s effects in a cancer context generally lean toward:
• Normalizing dysregulated calcium signaling to push cells toward apoptotic death
• Inhibiting pro-survival pathways such as PI3K/AKT/mTOR and NF-κB

(1) is essential for the growth and maintenance of bone;
(2) greatly improves wound healing;
(3) beneficially impacts the body's use of estrogen, testosterone, and vitamin D;
(4) boosts magnesium absorption;
(5) reduces levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor α (TNF-α);
(6) raises levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase;
(7) protects against pesticide-induced oxidative stress and heavy-metal toxicity;
(8) improves the brains electrical activity, cognitive performance, and short-term memory for elders;
(9) influences the formation and activity of key biomolecules, such as S-adenosyl methionine (SAM-e) and nicotinamide adenine dinucleotide (NAD(+));
(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
(11) may help ameliorate the adverse effects of traditional chemotherapeutic agents.

-Note half-life 21 hrs average
BioAv very high, 85-100%
Pathways:
- induce ROS productionin cancer cells, while reducing ROS in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑,(contrary) Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑,(contrary) HSP↓,
- Debateable if Lowers AntiOxidant defense in Cancer Cells: NRF2↓(most contrary), SOD↓(some contrary), GSH↓, Catalase↓(some contrary), HO1↓(contrary), GPx↓(some contrary)
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, IGF-1↓, VEGF↓, RhoA↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, P53↑, HSP↓,
- some indication of Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, ERK↓, EMT↓,
- small indication of inhibiting glycolysis : HIF-1α↓, cMyc↓, GRP78↑, Glucose↓,
- small indication of inhibiting angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


TumCMig, Tumor cell migration: Click to Expand ⟱
Source:
Type:
Tumor cell migration is a critical process in cancer progression and metastasis, which is the spread of cancer cells from the primary tumor to distant sites in the body.
Scientific Papers found: Click to Expand⟱
709- Bor,    Cellular changes in boric acid-treated DU-145 prostate cancer cells
- in-vitro, Pca, DU145
Cyc↓, dose-dependent reduction in cyclins A–E
MAPK↓,
TumCMig↓,
LAMP2↓,
p‑ERK⇅, Phosphorylated ERK (P-ERK1/2) increased at intermediate exposures (100 and 250 μM), relative to control, but was reduced by higher concentrations of BA
TumCM/A↑, BA induces media acidosis

702- Bor,  GEN,  SeMet,  Rad,    Evaluation of ecological and in vitro effects of boron on prostate cancer risk (United States)
- Analysis, NA, NA
Risk↓, Increased groundwater boron concentrations, across the state of Texas, correlate with reduced risk of prostate cancer incidence and mortality.
TumCMig↓, boric acid improves the anti-proliferative effectiveness of chemo-preventative agents, selenomethionine and genistein, while enhancing ionizing radiation cell kill
Bcl-2↓,

696- Bor,    Nothing Boring About Boron
- Review, Var, NA
*hs-CRP↓, reduces levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor μ (TNF-μ);
*TNF-α↓,
*SOD↑, raises levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase
*Catalase↑,
*GPx↑,
*cognitive↑, improves the brains electrical activity, cognitive performance, and short-term memory for elders; restricted boron intake adversely affected brain function and cognitive performance.
*memory↑, In humans, boron deprivation (<0.3 mg/d) resulted in poorer performance on tasks of motor speed and dexterity, attention, and short-term memory.
*Risk↓, Boron-rich diets and regions where the soil and water are rich in boron correlate with lower risks of several types of cancer, including prostate, breast, cervical, and lung cancers.
*SAM-e↑,
*NAD↝, Boron strongly binds oxidized NAD+,76 and, thus, might influence reactions in which NAD+ is involved
*ATP↝,
*Ca+2↝, Because of its positive charge, magnesium stabilizes cell membranes, balances the actions of calcium, and functions as a signal transducer
HDAC↓, some boronated compounds are histone deacetylase inhibitors
TumVol↓,
IGF-1↓, expression of IGF-1 in the tumors was significantly reduced by boron treatment
PSA↓, Boronic acid has been shown to inhibit PSA activity.
Cyc↓, boric acid inhibits the growth of prostate-cancer cells both by decreasing expression of A-E cyclin
TumCMig↓,
*serineP↓, Boron exists in the human body mostly in the form of boric acid, a serine protease inhibitor.
HIF-1↓, shown to greatly inhibit hypoxia-inducible factor (HIF) 1
*ChemoSideEff↓, An in vitro study found that boric acid can help protect against genotoxicity and cytotoxicity that are induced in lymphocytes by paclitaxel
*VitD↑, greater production of 25-hydroxylase, and, thus, greater potential for vitamin-D activation
*Mag↑, Boron significantly improves magnesium absorption and deposition in bone
*eff↑, boron increases the biological half-life and bioavailability of E2 and vitamin D.
Risk↓, risk of prostate cancer was 52% lower in men whose diets supplied more than 1.8 mg/d of boron compared with those whose dietary boron intake was less than or equal to 0.9 mg/d.
*Inflam↓, As research into the chemistry of boron-containing compounds has increased, they have been shown to be potent antiosteoporotic, anti-inflammatory, and antineoplastic agents
*neuroP↑, In addition, boron has anti-inflammatory effects that can help alleviate arthritis and improve brain function and has demonstrated such significant anticancer
*Calcium↑, increase serum levels of estradiol and calcium absorption in peri- and postmenopausal women.
*BMD↑, boron stimulates bone growth in vitamin-D deficient animals and alleviates dysfunctions in mineral metabolism characteristic of vitamin-D deficiency
*chemoP↑, may help ameliorate the adverse effects of traditional chemotherapeutic agents. boric acid can help protect against genotoxicity and cytotoxicity that are induced in lymphocytes by paclitaxel, an anticancer drug commonly used to treat breast, ovarian
AntiCan↑, demonstrated preventive and therapeutic effects in a number of cancers, such as prostate, cervical, and lung cancers, and multiple and non-Hodgkin’s lymphoma
*Dose↑, only an upper intake level (UL) of 20 mg/d for individuals aged ≥ 18 y.
*Dose↝, substantial number of articles showing benefits support the consideration of boron supplementation of 3 mg/d for any individual who is consuming a diet lacking in fruits and vegetables
*BMPs↑, Boron was also found to increase mRNA expression of alkaline phosphatase and bone morphogenetic proteins (BMPs)
*testos↑, 1 week of boron supplementation of 6 mg/d, a further study by Naghii et al20 of healthy males (n = 8) found (1) a significant increase in free testosterone,
angioG↓, Inhibition of tumor-induced angiogenesis prevents growth of many types of solid tumors and provides a novel approach for cancer treatment; thus, HIF-1 is a target of antineoplastic therapy.
Apoptosis↑, Cancer cells, however, commonly overexpress sugar transporters and/or underexpress borate export, rendering sugar-borate esters as promising chemopreventive agents
*selectivity↑, In normal cells, the 2 latter, cell-destructive effects do not occur because the amount of borate present in a healthy diet, 1 to 10 mg/d, is easily exported from normal cells.

722- Bor,    Boric acid as a promising agent in the treatment of ovarian cancer: Molecular mechanisms
- in-vitro, Ovarian, MDAH-2774
TumCP↓,
TumCI↓,
TumCMig↓,
Apoptosis↑,
ROS↑,
miR-21↓,
miR-130a↓,
Casp8∅, Caspase-8, Caspase-10, Cyclin D1, Cyclin D2, CDK6, CDK4, FADD, TRADD, FAS, DR4 and DR5 gene mRNA expression changes were found insignificant in boric acid treated group compared with control
Casp10∅,
cycD1∅,
CDK6∅,
CDK4∅,
FADD∅,
DR4∅,
DR5∅,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Results for Effect on Cancer/Diseased Cells:
angioG↓,1,   AntiCan↑,1,   Apoptosis↑,2,   Bcl-2↓,1,   Casp10∅,1,   Casp8∅,1,   CDK4∅,1,   CDK6∅,1,   Cyc↓,2,   cycD1∅,1,   DR4∅,1,   DR5∅,1,   p‑ERK⇅,1,   FADD∅,1,   HDAC↓,1,   HIF-1↓,1,   IGF-1↓,1,   LAMP2↓,1,   MAPK↓,1,   miR-130a↓,1,   miR-21↓,1,   PSA↓,1,   Risk↓,2,   ROS↑,1,   TumCI↓,1,   TumCM/A↑,1,   TumCMig↓,4,   TumCP↓,1,   TumVol↓,1,  
Total Targets: 29

Results for Effect on Normal Cells:
ATP↝,1,   BMD↑,1,   BMPs↑,1,   Ca+2↝,1,   Calcium↑,1,   Catalase↑,1,   chemoP↑,1,   ChemoSideEff↓,1,   cognitive↑,1,   Dose↑,1,   Dose↝,1,   eff↑,1,   GPx↑,1,   hs-CRP↓,1,   Inflam↓,1,   Mag↑,1,   memory↑,1,   NAD↝,1,   neuroP↑,1,   Risk↓,1,   SAM-e↑,1,   selectivity↑,1,   serineP↓,1,   SOD↑,1,   testos↑,1,   TNF-α↓,1,   VitD↑,1,  
Total Targets: 27

Scientific Paper Hit Count for: TumCMig, Tumor cell migration
4 Boron
1 Genistein
1 selenomethionine
1 Radiotherapy/Radiation
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:46  Target#:326  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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