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">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">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


Scientific Papers found: Click to Expand⟱
757- Bor,    Phenylboronic acid is a more potent inhibitor than boric acid of key signaling networks involved in cancer cell migration
- in-vitro, Pca, DU145 - in-vitro, Nor, RWPE-1
Rho↓, RhoA, but not in normal RWPE-1 prostate cells
Rac1↓, but not in normal RWPE-1 prostate cells
Cdc42↓, but not in normal RWPE-1 prostate cells
*eff↑, RhoA, Rac1, and Cdc42 activity is decreased in prostate cancer cells but not in normal prostate cells.

3502- Bor,    Plasma boron concentrations in the general population: a cross-sectional analysis of cardio-metabolic and dietary correlates
- Review, NA, NA
*Half-Life↑, half-life of circulating boron after dietary intake is about 21 h [7]
*VitD↑, hypothesized that boron supplementation increases the biological half-live and bioavailability of vitamin D [4].
*cardioP↑, cardio-metabolic correlates of plasma boron concentrations, these cardio-protective benefits might be (at least partially) mediated by boron.
*RenoP↓, higher concentrations of boron within the body in individuals with slightly reduced kidney function, than pointing towards a direct detrimental effect of boron on renal function.

768- Bor,    In vitro and in vivo antitumour effects of phenylboronic acid against mouse mammary adenocarcinoma 4T1 and squamous carcinoma SCCVII cells
- in-vitro, BC, 4T1
TumCP↓, most prominent antitumour effect was obtained by intraperitoneal administration, followed significantly by oral administration

767- Bor,    Boric acid induces cytoplasmic stress granule formation, eIF2α phosphorylation, and ATF4 in prostate DU-145 cells
- in-vitro, Pca, DU145
ER Stress↑,
eIF2α↑,
GRP78/BiP↑,
ATF4↑,

766- Bor,    In vitro effects of boric acid on human liver hepatoma cell line (HepG2) at the half-maximal inhibitory concentration
- in-vitro, Liver, HepG2
TumCCA↑,
DNAdam↑,
Apoptosis↑,

765- Bor,    High concentrations of boric acid induce autophagy in cancer cell lines
p62↓,
LC3II↑,
TumAuto↑,

764- Bor,    Effect of Tumor Microenvironment on Selective Uptake of Boric Acid in HepG2 Human Hepatoma Cells
- in-vitro, Liver, HepG2
BioAv↑, low pH and increased membrane fluidity, which are hallmarks of HCC, might further enhance BA uptake.

763- Bor,    Investigation of The Apoptotic and Antiproliferative Effects of Boron on CCL-233 Human Colon Cancer Cells
- in-vitro, Colon, CCl233
TumCP↓, 50 mM boric acid decreased cell proliferation after 24, 48 and 72 hours
PARP↓,
VEGF↓,

762- Bor,    Mechanism of boric acid cytotoxicity in breast cancer cell lines
- in-vitro, BC, MCF-7 - in-vitro, BC, ZR-75-1
TumCG↓, 68% inhibition of growth beginning on day 3 in ZR-75-1 cells and 70% inhibition of growth on day 5 in MCF-7.

761- Bor,    Prevalence of Prostate Cancer in High Boron-Exposed Population: A Community-Based Study
other↓, prostatic volumes in men whose prostates were biopsied (p < 0.012) was significantly lower in the study group as compared with those in the control group 2

760- Bor,    Therapeutic Efficacy of Boric Acid Treatment on Brain Tissue and Cognitive Functions in Rats with Experimental Alzheimer’s Disease
- in-vivo, AD, NA
*memory↑, BA reduced damage to learning and memory functions and significantly lowered oxidative stress markers in the AD model.
*ROS↓, been reported that BA also reduces oxidative stress by increasing glutathione reserves,
*GSH↑,
*Aβ↓, and strongly inhibits Aβ aggregation via hydroxyl group
*Inflam↓, BA can act as a protective agent in apoptotic processes by regulating oxidative and inflammatory processes as well as mitochondrial membrane potential
*MMP↑,
*lipid-P↓, BA added to the diet prevented lipid peroxidation by supporting and strengthening the antioxidant defense system.
*Ca+2↓, Boron is thought to prevent apoptosis and strengthen antioxidant defense by reducing intracellular oxygen radicals and calcium levels.
*cognitive↑, Our hypothesis is that boric acid can improve cognitive function and histopathological outcomes by reducing oxidative stress in rats with STZ-induced Alzheimer’s Disease
*TOS↓, After BA administration, it increased TAS by increasing the antioxidant effect, and as a result, TOS and OSI decreased.

759- Bor,    The nutritional and metabolic effects of boron in humans and animals
- in-vivo, NA, NA
DHT↑, testosterone
VitD↑,
HDL↓,

758- Bor,    Comparative effects of daily and weekly boron supplementation on plasma steroid hormones and proinflammatory cytokines
- Human, NA, NA
*hs-CRP↓, Six hours supplementation showed a significant decrease on sex hormone binding globulin (SHBG), high sensitive CRP (hsCRP) and TNF-α level.
*TNF-α↓,
*SHBG↓,
*DHT↑, Dihydrotestosterone, cortisol and vitamin D was elevated.
*cortisol↑,
*VitD↑,
*BioAv↑, 11.6 mg of boron resulted in a significant increase in plasma boron concentration. Given such a fast bioavailabilit
*Inflam↓, Also, concentrations of all three inflammatory biomarkers decreased after supplementation.

3503- Bor,    Chemical disposition of boron in animals and humans
- Review, NA, NA
*Half-Life↑, The half-life of boric acid in humans is on the order of 1 day. They also infused 600 mg of boric acid into seven human subjects and calculated a mean half-life of 21 hr.
*other↑, Bone contained the highest level of boron of any tissue. After only 1 day on the diet, the boron content of bone increased 20-fold.

756- Bor,    Evaluation of Boric Acid Treatment on microRNA‐127‐5p and Metastasis Genes Orchestration of Breast Cancer Stem Cells
- in-vitro, BC, MCF-7
COL1A1↓,
Vim↓,
miR-127-5p↑,
Zeb1↑, expression of the miR-127-5p, ZEB1, CDH1, ITGB1 , ITGA5 , LAMA5 , and SNAIL, was up-regulated in dose-treated BC-SCs
CDH1↑,
ITGB1↑,
ITGA5↑,
LAMA5↑,
Snail↑,

755- Bor,    https://aacrjournals.org/cancerres/article/67/9_Supplement/4220/535557/Boric-acid-induces-apoptosis-in-both-prostate-and
- in-vitro, Pca, DU145 - in-vitro, PC, PC3
TumCG↓, but not MDA-MB-231, MDA-MB-435, T-47D
 >or MCF-7 breast cancer cell lines
Apoptosis↑,

754- Bor,  HRT,    Dietary Boron and Hormone Replacement Therapy as Risk Factors for Lung Cancer in Women
- Analysis, NA, NA
Risk↓, Boron intake was inversely associated with lung cancer in women, whereas women who consumed low boron and did not use HRT were at substantial increased odds

753- Bor,    Boron Intake and decreased risk of mortality in kidney transplant recipients
OS↑, Boron may be an overlooked target to improve long-term survival among KTR and potentially other patients

752- Bor,    The Potential Role of Boron in the Modulation of Gut Microbiota Composition: An In Vivo Pilot Study
GutMicro↑, Notable increases in genera like Treponema and Catellicoccus were observed, suggesting the potential of boron compounds to enrich microbial communities with unique metabolic functions

751- Bor,  5-FU,    Cytotoxic and Apoptotic Effects of the Combination of Borax (Sodium Tetraborate) and 5-Fluorouracil on DLD-1 Human Colorectal Adenocarcinoma Cell Line
- in-vitro, CRC, DLD1
Apoptosis↑, combination of borax with 5-FU has a strong cytotoxic and apoptotic effect on the human CRC DLD-1 cells.

750- Bor,    Calcium fructoborate regulate colon cancer (Caco-2) cytotoxicity through modulation of apoptosis
- in-vitro, CRC, Caco-2
Bcl-2↓,
BAX↑,
Akt↓,
p70S6↓,
PTEN↑,
TSC2↑,

749- Bor,    Comparative effects of boric acid and calcium fructoborate on breast cancer cells
P53↓, CF but not BA
Bcl-2↓, CF but not BA
Casp3↑,
Apoptosis↑,

748- Bor,    A Study on the Anticarcinogenic Effects of Calcium Fructoborate
- in-vitro, BC, MDA-MB-231
p‑ATM↑,
p‑P53↑,
Casp9↑,
PARP↓, 2.5 fold decrease
VEGF↓,
Casp3↑, 50 μM CaFB only

747- Bor,    Growing Evidence for Human Health Benefits of Boron
- Review, NA, NA
TumCG↓, 1mmol/L
Risk↓, boron intake was inversely associated with the incidence of cancer

746- Bor,    Organoboronic acids/esters as effective drug and prodrug candidates in cancer treatments: challenge and hope
- Review, NA, NA
eff↑, newly developed boron-containing compounds have already demonstrated highly promising activities
*toxicity↓, Boronic acid/ester has been successfully incorporated into cancer treatments and therapy mainly due to its remarkable oxophilicity and low toxicity levels in the body
ROS↑, can trigger tumour microenvironmental abnormalities such as high levels of reactive oxygen species (ROS) and overexpressed enzymes
LAT↓, boron accumulation were observed to counterpart LAT-1 expression in a bone metastasis model of breast cancer
AntiCan↑, high concentration of boron in males reduces the probability of prostate cancer by 54% compared to males with low boron concentrations
AR↓, bortezomib
PSMB5↓, bortezomib
IGF-1↓, insulin-like growth factor 1 (IGF-1) in tumours was markedly reduced by boric acid.
PSA↓, exposure to both low-and high-dose boron supplementation, prostate-specific antigen (PSA) levels dropped by an average of 87%, while tumour size declined by an average of 31.5%
TumVol↓,
eff↑, phenylboronic acid is a more potent inhibitor than boric acid in targeting metastatic and proliferative properties of prostate cancer cells
Rho↓, RhoA, Rac1
Cdc42↓,
Ca+2↓, ER Ca+2 depletion occurred after the treatment of DU-145 prostate cancer cells with the physiological concentrations of boric acid
eff↑, boric acid (BA), sodium pentaborate pentahydrate (NaB), and sodium perborate tetrahydrate (SPT) against SCLC cell line using DMS-114 cells

3515- Bor,    EVIDENCE THAT BORON DOWN-REGULATES INFLAMMATION THROUGH THE NF-(KAPPA)B PATHWAY
- in-vitro, Nor, NA
*TNF-α↓, supplemental boron displayed decreased levels of TNF-alpha (a), IL-1ß, MIP-1a, and iNOS expression. Each of these factors is under NF-kappa (k) B control.
*IL1β↓,
*MIP‑1α↓,
*iNOS↓,
*NF-kB↓,

3527- Bor,    The potential role of borophene as a radiosensitizer in boron neutron capture therapy (BNCT) and particle therapy (PT)
- NA, Var, NA
RadioS↑, This study lays a foundation for utilizing novel borophene-based nanomaterials as radiosensitizers as well as imaging probes in cancer treatment.

3525- Bor,    Synthesis of DNA-Boron Cluster Composites and Assembly into Functional Nanoparticles with Dual, Anti-EGFR, and Anti-c-MYC Oncogene Silencing Activity
- in-vitro, PC, PANC1
EGFR↓, The nanoparticles exhibited notable silencing efficiency in vitro in a pancreatic carcinoma cell line PANC-1 toward EGFR and c-Myc genes at the mRNA level, and a significant efficiency at the protein level.
cMyc↓,

3524- Bor,    Boric Acid Alleviates Lipopolysaccharide-Induced Acute Lung Injury in Mice
*Inflam↓, Furthermore, BA exhibited anti-inflammatory properties by suppressing inflammatory cytokines within the lung tissue.
*SOD↑, BA ingestion caused upregulation in SOD and a decrease in MDA contents in lung tissue homogenates.
*MDA↓,
*GRP78/BiP↓, BA downregulated the levels of GRP78 and CHOP compared to the LPS group.
*CHOP↓,
*NRF2↑, Remarkably, BA also upregulated transcription and protein expression of Nrf2 and HO-1 compared to the LPS group.
*HO-1↑,

3523- Bor,    Design, Synthesis, and Biological Activity of Boronic Acid-Based Histone Deacetylase Inhibitors
- in-vitro, Var, NA
HDAC↓, In cancer cell growth inhibition assays, compounds (S)-18, 20, and 21 exerted strong activity, and the values of the ratio of the concentration causing 50% growth inhibition (GI50) to the concentration causing 50% enzyme inhibition

3522- Bor,    The Boron Advantage: The Evolution and Diversification of Boron’s Applications in Medicinal Chemistry
- Review, Var, NA
Hif1a↓, One compound, GN26361 (Table 2), potently inhibited the accumulation of HIF-1α under hypoxic conditions via the inhibition of hypoxia-induced HIF-1α transcriptional activity in HeLa cells (IC50 = 0.74 μM) [54].
HDAC↓, Peptidic boronic acids have also been studied for other microbial targets including as a hepatitis C virus (HCV) NS3/4A protease inhibitor [55], an antitubercular drug [56], penicillin-binding proteins [57], histone deacetylase (HDAC) inhibitors [58]
*CXCR2↑, reported boronic acid chemokine antagonist for CXCR 1 and 2 and was able to significantly inhibit inflammation in vivo
ROS↑, In addition to being used as ROS-activated prodrugs, boron-containing drugs have also been modified to form a prodrug, with the intention of increasing the favourability of their pharmacokinetic properties.

3521- Bor,    A new hope for obesity management: Boron inhibits adipogenesis in progenitor cells through the Wnt/β-catenin pathway
- in-vitro, Obesity, 3T3
*CEBPA↓, Figure 2
*PPARγ↓,
*FASN↓,
*SREBP1↓,
*FABP4↓,
*GLUT4↓,
*β-catenin/ZEB1↑, Boron Activated the β-Catenin Signaling Pathway
*MMP2↓, As shown in Fig. 6, soluble transforming growth factor receptor 1 (sTNFR1) and matrix metalloproteinase 2 (MMP2) protein levels decreased in the presence of boron
*FGF↑, whereas basic fibroblast growth factor expression (bFGF) increased
*Ca+2?, Boric acid has been reported to interact with NAD + and inhibit cyclic ADP ribose-activated Ca 2+ release from ryanodine receptor, leading to decreased endoplasmic reticulum luminal Ca 2+ concentrations

3520- Bor,    Effect of boron element on photoaging in rats
- in-vivo, NA, NA
*hepatoP↑, to positively affect the liver metabolism, and to promote bone density, embryogenic development and wound healing, and is known to provide significant benefits in cancer treatment through neutron capture systems
*BMD↑,
*COX2↓, Increased skin inflammatory parameters (COX-2, IL-8, NF-KB, IL-6, and TNF-α) levels in UVB-exposed groups were inhibited in all treatment groups
*IL8↓,
*NF-kB↓,
*IL6↓,
*TNF-α↓,

3519- Bor,    Boron-Based Inhibitors of the NLRP3 Inflammasome
- Review, NA, NA
NLRP3↓, Establishing the Importance of Boron in 2APB for NLRP3 Inflammasome Inhibition

3518- Bor,    Boron Report
- Review, Var, NA - Review, AD, NA
Risk↓, Boron reduces prostate cancer incidence by up to 64%
serineP↓, Boric acid acts to inhibit serine proteases—it decreases PSA by 87% and reduces tumor size in a prostate cancer mouse model
PSA↓,
TumVol↓,
IGF-1↓, expression of IGF-1 (insulin-like growth factor type 1) was markedly reduced by boron treatment. Circulating blood levels of IGF-1 were not reduced in the treated mice, however.
*Mag↑, In situations of adequate calcium supply but deficient magnesium resources, boron appears to substitute or “pinch hit” for magnesium during the process of bone formation.
*Calcium↑, The effect of boron on raising plasma calcium levels may, in part, be due to its enhancing effect on vitamin D.1
*VitD↑,
*COX2↓, boron has been shown to inhibit cyclooxygenase (COX) and lipoxygenase (LOX).
*5LO↓,
*PGE2↓, leads to a decrease in prostaglandin E2 (PGE2)
*NF-kB↓, suppressing nuclear factor kappa beta (NfkappaB)
*cognitive↑, Since it is now commonly accepted that the routine use of NSAIDs significantly reduces the incidence of Alzheimer’s disease,31,32 it is not surprising that papers have been published on boron’s positive effect on cognitive function.

3517- Bor,  Se,    The protective effects of selenium and boron on cyclophosphamide-induced hepatic oxidative stress, inflammation, and apoptosis in rats
- in-vivo, Nor, NA
*hepatoP↑, However, it was found that Se protects the liver slightly better against CP damage than B
*ALAT↓, statistically significant difference was observed in the serum levels of ALT, AST, ALP, TAS, TOS and OSI.
*AST↓,
*ALP↓,
*NF-kB↓, A statistically significant difference was observed in serum levels of NF-kB, TNF-α, IL -1β, IL -6 and IL -10 when the Se + CP and B + CP-treated groups were compared with the CP-treated group
*TNF-α↓, fig 9
*IL1β↓,
*IL6↓,
*IL10↑,
*SOD↑, A statistically remarkable change in serum levels of SOD, CAT, GPx, MDA and GSH was observed in the group receiving only CP compared to groups Se, B and the control.
*Catalase↑,
*MDA↓, Fig 10
*GSH↑,
*GPx↑,
*antiOx↑, suggests that B and Se increase intracellular antioxidant status.
*NRF2↑, Se and B treatment can protect rat liver tissue from CP-induced oxidative stress, inflammation, and apoptosis by regulating Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways.
*Keap1↓,

3516- Bor,    Boron in wound healing: a comprehensive investigation of its diverse mechanisms
- Review, Wounds, NA
*Inflam↓, anti-inflammatory, antimicrobial, antioxidant, and pro-proliferative effects.
*antiOx↑,
*ROS↓, The antioxidant properties of boron help protect cells from oxidative stress, a common feature of chronic wounds that can impair healing
*angioG↑, Boron compounds exhibit diverse therapeutic actions in wound healing, including antimicrobial effects, inflammation modulation, oxidative stress reduction, angiogenesis induction, and anti-fibrotic properties.
*COL1↑, Boron has been shown to increase the expression of proteins involved in wound contraction and matrix remodeling, such as collagen, alpha-smooth muscle actin, and transforming growth factor-beta1.
*α-SMA↑,
*TGF-β↑,
*BMD↑, Animals treated with boron showed favorable changes in bone density, wound healing, embryonic development, and liver metabolism
*hepatoP↑,
*TNF-α↑, BA elevates TNF-α and heat-shock proteins 70 that are related to wound healing.
*HSP70/HSPA5↑,
*SOD↑, antioxidant properties of BA showed that boron protects renal tissue from I/R injury via increasing SOD, CAT, and GSH and decreasing MDA and total oxidant status (TOS)
*Catalase↑,
*GSH↑,
*MDA↓,
*TOS↓,
*IL6↓, Boron supports gastric tissue by alleviating ROS, MDA, IL-6, TNF-α, and JAK2/STAT3 action, as well as improving AMPK activity
*JAK2↓,
*STAT3↓,
*AMPK↑,
*lipid-P↓, boron may improve wound healing by hindering lipid peroxidation and increasing the level of VEGF
*VEGF↑,
*Half-Life↝, Boron is a trace element, usually found at a concentration of 0–0.2 mg/dL in plasma with a half-life of 5–10 h, and 1–2 mg of it is needed in the daily diet

745- Bor,    Investigation of cytotoxic antiproliferative and antiapoptotic effects of nanosized boron phosphate filled sodium alginate composite on glioblastoma cancer cells
- in-vitro, GBM, U87MG - in-vitro, Nor, L929 - in-vitro, GBM, T98G
TumCD↑,
*toxicity↓, did not affect healthy fibroblast cells but had a cytotoxic effect on glioblastoma cells

3514- Bor,  CUR,    Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta
- in-vivo, AD, NA
*DNAdam↓, Co-administration of BA and curcumin on synaptosomes exposed to Aβ1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities.
*MDA↓,
*AChE↓,
*neuroP↑, BA and curcumin had protective effects on rat brain synaptosomes against Aβ1-42 exposure.
*ROS↓, BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of Aβ1-42 exposed.
*NO↓, Synaptosomes treated with BA showed a significant reduction in MDA and NO levels

3513- Bor,    Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status
- in-vitro, Pca, DU145 - in-vitro, Nor, MEF
NRF2↑, Cytoplasmic Nrf2 was translocated to the nucleus at 1.5–2 h in DU-145 and MEF WT cells, but not MEF PERK −/− cells. BA treatment demonstrating BA-activated Nrf2
selectivity↑, but not MEF PERK −/− cells.
NQO1↑, , NQO1, GCLC, and HMOX-1. DU-145 cells treated with BA increased the expression of all three gene
GCLC↑,
HO-1↑,
TumCP↓, BA activates Nrf2 and ARE explains how BA slows proliferation of DU-145 cells but does not cause apoptosis

3512- Bor,    Activation 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 Intake
- in-vitro, Pca, DU145
TumCP↓, Treatment of DU-145 prostate cancer cells with physiological concentrations of BA inhibits cell proliferation without causing apoptosis and activates eukaryotic initiation factor 2 (eIF2α).
eIF2α↑, Phosphorylation of eIF2α occurs following BA treatment of DU-145 and LNCaP prostate cells
ATF4↑, post-treatment increases in eIF2α protein at 30 min and ATF4 and ATF6 proteins at 1 h and 30 min, respectively
ATF6↑,
GADD34↑, The increase in ATF4 was accompanied by an increase in the expression of its downstream genes growth arrest and DNA damage-induced protein 34 (GADD34) and homocysteine-induced ER protein (Herp),
CHOP↓, but a decrease in GADD153/CCAAT/enhancer-binding protein homologous protein (CHOP), a pro-apoptotic gene.
GRP78/BiP↑, The increase in ATF6 was accompanied by an increase in expression of its downstream genes GRP78/BiP, calreticulin, Grp94, and EDEM.
GRP94↑,
Risk↓, Low boron status has been associated with increased cancer risk, low bone mineralization, and retinal degeneration
*BMD↑,
Ca+2↓, LNCaP and DU-145: BA binds to cADPR and inhibits cADPR-activated Ca2+ release from the endoplasmic reticulum (ER) in a dose-dependent manner [15, 16] and lowers ER luminal Ca2+ concentrations
*Half-Life↝, lood levels of BA are dynamic, rising rapidly after a meal with an elimination half-life from 4 to 27.8 h depending on dose
IRE1∅, BA does not activate IRE1
chemoP↑, Dietary boron has been connected to three seemingly unconnected observations, increased bone mass and strength [10, 74, 75], chemoprevention

3511- Bor,    Boron
- Review, NA, NA
*memory↑, In boron-deprived humans, boron supplementation improved mental alertness, attention, short-term memory, and motor speed and dexterity.
*motorD↑,
*neuroP↑,
Ca+2↓, human prostate cells, boric acid acts as a reversible noncompetitive inhibitor of cADPR leading to decreased endoplasmic reticulum Ca2+
ATF4↑, The decreased Ca2+ results in the E74 like ETS transcription factor 2α activating transcription factor 4 (ATF4) and nuclear factor erythroid 2 like 2 (Nrf2),
NRF2↑,
*Inflam↓, a dietary boron intake >0.4 mg/d may be useful for bone and brain health and in modulating inflammatory and oxidative stress
*ROS↓,

3510- Bor,    Boron Affects the Development of the Kidney Through Modulation of Apoptosis, Antioxidant Capacity, and Nrf2 Pathway in the African Ostrich Chicks
- in-vivo, Nor, NA
*RenoP↑, Our results revealed that low doses of boron (up to 160 mg) had positive effect, while high doses (especially 640 mg) caused negative effect on the development of the kidney
*ROS↓, The low doses regulate the oxidative and enzyme activity in the kidney.
*antiOx↑, boron at low doses upregulated the expression of genes involved in the antioxidant pathway
*Apoptosis↓, low levels of boron (up to 160 mg) inhibited the cell apoptosis, regulate the enzyme activity, and improved the antioxidant system, thus may encourage the development of the ostrich chick's kidney
*NRF2↑, maximum localization of Nrf2 in 80 mg/L BA dose group
*HO-1↑, As the boron concentration increased, the expression of Nrf2, GCLc, and HO-1 genes upregulated
*MDA↓, In comparison to those of the group 1, MDA content (lipid peroxidation marker) was significantly decreased by 26.02 and 48.12% in the 40 and 80 mg/L BA groups
*lipid-P↓,
*GPx↓, GSH-PX activity of ostrich chick kidney tissue was slightly increased in the 40 and 80 mg/L BA groups,
*Catalase↑, supplementation of low doses of boron in the ostrich drinking water has resulted in stimulation of antioxidant capacity of GR, CAT, and SOD significantly.
*SOD↑,
*ALAT↓, boron supply in low doses (especially 80 mg/L BA) showed decrease levels in the activity of ALT, AST, and ALP.
*AST↓,
*ALP↓,

3509- Bor,    Boron and Prostate Cancer a Model for Understanding Boron Biology
- NA, Pca, NA
Ca+2↓, boric acid inhibits calcium (Ca²+) release from the endoplasmic reticulum. NAD+ stimulated release of Ca2+ was greatly diminished in the presence of boric acid

3508- Bor,    The Effect of Boron on the UPR in Prostate Cancer Cells is Biphasic
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
ER Stress↑, Treatment with 250 uM B induced endoplasmic reticulum (ER) stress in androgen dependent LNCaP and androgen independent DU-145 prostate cancer cell lines.
GRP78/BiP↑, this treatment induced BiP/GRP78, calreticulin and phosphorylation of eif2α the hallmarks of the unfolded protein response (UPR).
p‑eIF2α↑,
UPR↑,
eff↓, In contrast, concentrations of 1 uM B and 10 uM B rescued DU-145 cells respectively treated with 120 uM tunicamycin or 10 uM thapsigargin to induce ER stress.

3507- Bor,    Boron inhibits apoptosis in hyperapoptosis condition: Acts by stabilizing the mitochondrial membrane and inhibiting matrix remodeling
*MMP↑, n the presence of boron, there was a significant and dose-dependent increase in MMP, which inhibited mitochondrial remodeling to the condensed state and hence the release of Cyt c and initiation of apoptosis.
*Cyt‑c↓, Boron inhibits the release of mitochondrial Cyt c and activation of Casp
*Apoptosis↓, Boron inhibits apoptosis.
*Casp3↓,
*NO↓, Nitric oxide (NO) and iNOS levels decrease in boron treated hyperapoptosis cultures.
*iNOS↓,

3506- Bor,    Boron Chemistry for Medical Applications
- Review, NA, NA
radioP↑, These properties enable alpha particles tagged with B-10 to selectively kill various types of cancer cells without damaging the normal cells, that helps to prevent the side effects for patients.
selectivity↑,

3505- Bor,    Mineral requirements for mitochondrial function: A connection to redox balance and cellular differentiation
- Review, NA, NA
*glucose↓, Boron supplementation in human subjects decreased serum glucose, creatinine, and calcitonin,
*creat↓,
*SOD↑, while it increased serum triglycerides, ceruloplasmin, and erythrocyte superoxide dismutase
*MMP↑, Boron administration had positive effects on mitochondrial membrane potential and function in multiple species, but entry into mitochondria was not confirmed
*ROS↓, The available evidence suggest that mitochondria may benefit from the availability of boron, which may promote metabolism and reduce redox stress.

3504- Bor,    Boron Contents of German Mineral and Medicinal Waters and Their Bioavailability in Drosophila melanogaster and Humans
- Review, NA, NA
other↑, Overall, current data demonstrate that water in Germany varies significantly in the content of boron and that only boron-rich mineral water improves the boron status in both flies and humans.
BioAv↑, Moreover, the consumption of HB mineral water led to an increase in serum boron concentrations up to 72 ± 5.8 µg L−1 and a subsequent decline over 24 h to final circulating boron levels that were again comparable to baseline values.

708- Bor,    Boron containing compounds as protease inhibitors
PSA↓,

720- Bor,    High Concentrations of Boric Acid Trigger Concentration-Dependent Oxidative Stress, Apoptotic Pathways and Morphological Alterations in DU-145 Human Prostate Cancer Cell Line
- in-vitro, Pca, DU145
ROS↑, boric acid, known as an antioxidant, may prevent cell proliferation by acting as an oxidant in certain doses
TumCG↓,
Apoptosis↑,

719- Bor,    Boric Acid Affects Cell Proliferation, Apoptosis, and Oxidative Stress in ALL Cells
- in-vitro, ALL, NA
Apoptosis↑,
miR-21↓,
TOS↓, while decreasing TOS levels in Jurkat cells

718- Bor,    Boric Acid Exhibits Anticancer Properties in Human Endometrial Cancer Ishikawa Cells
- in-vitro, NA, NA
OSI↑, decreased in healthy cells ****
TNF-α↓,
IL1↓, IL-1β
Casp3↑,
Apoptosis↑,
TOS↑, increased in Ishikawa cells but decreased in healthy cells ****

717- Bor,  PacT,    Boric acid as a protector against paclitaxel genotoxicity
- in-vitro, NA, NA
ChemoSideEff↓, PAC-induced increases in the genotoxicity and cytotoxicity indices were diminished by the addition of BA

716- Bor,    Sugar-borate esters--potential chemical agents in prostate cancer chemoprevention
TumCG↓, leads to growth inhibition and apoptosis
Apoptosis↑,

715- Bor,    Boron-containing phenoxyacetanilide derivatives as hypoxia-inducible factor (HIF)-1alpha inhibitors
- in-vitro, Pca, HeLa
Hif1a↓,

714- Bor,    Dietary Boron and Hormone Replacement Therapy as Risk Factors for Lung Cancer in Women
- Analysis, NA, NA
Risk↓, Boron intake was inversely associated with lung cancer in women, whereas women who consumed low boron and did not use HRT were at substantial increased odds.

713- Bor,    Effects of dietary boron on cervical cytopathology and on micronucleus frequency in exfoliated buccal cells
- Analysis, NA, NA
Risk↓, suggested that higher amounts of boron in drinking water may help inhibit HPV transformation, reducing incidence of cervical cancer.

712- Bor,    Boron concentrations in selected foods from borate-producing regions in Turkey
- Analysis, NA, NA
Risk↓, in Turkey, it has been suggested that the low incidence of cervical cancer in Turkey correlates with its boron-rich soil

711- Bor,    Receptor Activated Ca2+ Release Is Inhibited by Boric Acid in Prostate Cancer Cells
- in-vitro, Pca, DU145
Ca+2↓, exposure of DU-145 cells to 50 µM BA for 1 hr decreased stored [Ca2+] by 32%.

710- Bor,    Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells
- in-vitro, Pca, DU145
NAD↓, inhibits NAD+ and NADP+
TumCP↓, Cell proliferation was inhibited by 30% at 100 microM, 60% at 250 microM, and 97% at 1,000 microM BA
CD38↑,
Ca+2↓, hypothesize that toxicity of BA stems from the ability of high concentrations to impair Ca2+ signaling.

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

721- Bor,    Polymers Based on Phenyl Boric Acid in Tumor-Targeted Therapy
- Analysis, NA, NA
SA↓, Phenyl Boric Acid (PBA) can specifically bind to SA

707- Bor,    Cytotoxic and apoptotic effects of boron compounds on leukemia cell line
- in-vitro, AML, HL-60
Apoptosis↑, apoptotic effect was found at a concentration of 1,000 µM concentration in normal lymphocytes and HL-60 (acute leukemia cells) cells (2.5 % and 8.8 % respectively).

706- Bor,    Boron supplementation inhibits the growth and local expression of IGF-1 in human prostate adenocarcinoma (LNCaP) tumors in nude mice
- in-vivo, Pca, LNCaP
TumVol↓, 38%
IGF-1↓, in tumors
PSA↓, 89%

705- Bor,    Boric acid inhibits human prostate cancer cell proliferation
- in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP
TumCP↓,

704- Bor,    Inhibition of the enzymatic activity of prostate-specific antigen by boric acid and 3-nitrophenyl boronic acid
- in-vitro, Pca, NA
PSA↓, PSA activity is inhibited in vitro by boric acid

703- Bor,    Boron intake and prostate cancer risk
- Analysis, NA, NA
Risk∅, No correlation with prostate cancer frequency has been observed when boron consumption was less than 1.17 mg/d.

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↓,

701- Bor,    Dietary boron intake and prostate cancer risk
- Analysis, NA, NA
Risk↓, increased dietary boron intake was associated with a decreased risk of prostate cancer with a dose-response pattern.

700- Bor,    Diadenosine phosphates and S-adenosylmethionine: novel boron binding biomolecules detected by capillary electrophoresis
- Analysis, NA, NA
SAM-e↝,

699- Bor,    Boric Acid Alleviates Gastric Ulcer by Regulating Oxidative Stress and Inflammation-Related Multiple Signaling Pathways
- in-vivo, NA, NA
*ROS↓,
*MDA↓,
*TNF-α↓,
*IL6↓,
*JAK2↓,
*STAT3↓,
*AMPK↑,
*Sema3A/PlexinA1↑,

698- Bor,    Boron deprivation decreases liver S-adenosylmethionine and spermidine and increases plasma homocysteine and cysteine in rats
- in-vitro, NA, NA
SAM-e↑,

697- Bor,    Boron-containing compounds as preventive and chemotherapeutic agents for cancer
- Review, NA, NA
serineP↓,
NADHdeh↓,
Apoptosis↑,

733- Bor,    The analysis of boric acid effect on epithelial-mesenchymal transition of CD133 + CD117 + lung cancer stem cells
- in-vitro, Lung, NA
Snail↑,
ITGB1↑,
ITGA5↑,
COL1A1↓, 50 mM 24 h of BA treatment could be more beneficial as it reduces the expression of COL1A1 in cancer stem cells.
LAMA5↑,
MMP3↓,
Vim↓,
E-cadherin↑,
EMT↓, inhibit the EMT of lung cancer stem cells by reducing E-cadherin and Collagen-1 expression.
Zeb1↑,

744- Bor,    Borax affects cellular viability by inducing ER stress in hepatocellular carcinoma cells by targeting SLC12A5
- in-vitro, HCC, HepG2 - in-vitro, Nor, HL7702
TumCCA↑, cell cycle arrest in the G1/G0 phase
SLC12A5↓,
ATF6↑,
CHOP↑,
GRP78/BiP↑,
Casp3↑,
ER Stress↝,
*toxicity↓, HL‐7702 cells(normal) treated with 22.6 and 45.7 mM borax for 24 h showed no notable abnormalities in cellular size and cytoplasmic volume compared to the control group
*eff↓, tumour blood vessels absorb much higher levels of boric acid than normal liver tissues

743- Bor,    Boric Acid (Boron) Attenuates AOM-Induced Colorectal Cancer in Rats by Augmentation of Apoptotic and Antioxidant Mechanisms
- in-vitro, CRC, NA
BAX↑,
Bcl-2↓,
GPx↑,
SOD↑,
Catalase↑,
MDA↓, in colon tissue homogenates
TNF-α↓,
IL6↓,
IL10↑,

742- Bor,    In Vitro Effects of Boric Acid on Cell Cycle, Apoptosis, and miRNAs in Medullary Thyroid Cancer Cells
- in-vitro, Thyroid, NA
NOXA↑,
APAF1↑,
BAX↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Bcl-xL↓,
miR-21↓,

741- Bor,    Boron Derivatives Inhibit the Proliferation of Breast Cancer Cells and Affect Tumor-Specific T Cell Activity In Vitro by Distinct Mechanisms
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
MOB1↓,
PD-L1↑,
p‑YAP/TEAD↝,
IFN-γ↓,
sFasL↑,
Perforin↓,
GranA↓,
GranB↓,
GNLY↓,
PD-1↑, increased the expression of PD-1 surface protein in activated T cells

740- Bor,    Anti-cancer effect of boron derivatives on small-cell lung cancer
- in-vitro, Lung, DMS114 - in-vitro, Nor, MRC-5
Apoptosis↑, apoptosis increased by 10, 19, and 42 percent after treatment with BA, NaB, and SPT for 72 h, respectively
TumCCA↑,
P53↑,
Casp3↑,
*toxicity↓, without damaging normal MRC-5 cells

739- Bor,    Borax regulates iron chaperone- and autophagy-mediated ferroptosis pathway in glioblastoma cells
- in-vitro, GBM, U87MG - in-vitro, Nor, HMC3
TumCG↓,
TumCP↓,
TumCCA↑, remarkably reduced S phase in the U87-MG cells (opposite on normal cells)
PCBP1↓,
GSH↓,
GPx4↓,
Beclin-1↑,
MDA↑,
ACSL4↑,
Casp3↑,
Casp7↑,
Ferroptosis↑,
*toxicity↓, exhibited selectivity by having an opposite effect on normal cells (HMC3).

738- Bor,    Borax induces ferroptosis of glioblastoma by targeting HSPA5/NRF2/GPx4/GSH pathways
- in-vitro, GBM, U251 - in-vitro, GBM, A172 - in-vitro, Nor, SVGp12
TumCP↓,
GPx4↓, borax treatment decreased GPx4, GSH, HSPA5 and NRF2 levels in U251 and A172 cells while increasing MDA levels and caspase‐3/7 activity.
GSH↓,
HSP70/HSPA5↓,
NRF2↓,
MDA↑,
Casp3↑,
Casp7↑,
Ferroptosis↑, Consequently, borax may induce ferroptosis in GBM cells
selectivity↑, Treating SVG cells with borax concentrations ranging from 0 to 800 μM for 24 h did not result in a significant reduction in viability compared to the control group

737- Bor,    Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Statu
- in-vitro, Pca, DU145
Risk↓, intake is associated with reduced risk of cancer and DNA damage and increased antioxidant status.
p‑eIF2α↑,
ATF4↑,
GADD34↑,

736- Bor,    Evaluation of Boric Acid Treatment on microRNA-127-5p and Metastasis Genes Orchestration of Breast Cancer Stem Cells
- in-vitro, BC, MCF-7
miR-126↑, boric acid could induce miR-127-5p expression
COL1A1↓,
Vim↓,
Zeb1↑, expression of the miR-127-5p, ZEB1, CDH1, ITGB1, ITGA5, LAMA5, and SNAIL, was up-regulated in dose-treated BC-SCs
CDH1↑,
ITGB1↑,
ITGA5↑,
LAMA5↑,
Snail↑,
miR-127-5p↑,

735- Bor,    Boric Acid Alters the Expression of DNA Double Break Repair Genes in MCF-7-Derived Breast Cancer Stem Cells
- in-vitro, BC, NA
BRCA1↑,
BRCA2↑,
ATM↓,

734- Bor,    Boric Acid Affects the Expression of DNA Double-Strand Break Repair Factors in A549 Cells and A549 Cancer Stem Cells: An In Vitro Study
- in-vitro, Lung, A549
ATM↓, 30x
Casp3↑,
E-cadherin↑,

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.

732- Bor,    Boron's neurophysiological effects and tumoricidal activity on glioblastoma cells with implications for clinical treatment
eff↑, many boron compounds possess direct tumoricidal activity and there is substantial evidence that certain boron compounds can cross the blood-brain barrier.
IGF-1↝,
Glycolysis↝,

731- Bor,    Protective Effect of Boric Acid Against Ochratoxin A-Induced Toxic Effects in Human Embryonal Kidney Cells (HEK293): A Study on Cytotoxic, Genotoxic, Oxidative, and Apoptotic Effects
- in-vitro, Nor, HEK293
*ROS↓, normal kidney cells with Ochratoxin A-Induced Toxic Effects

730- Bor,  Cisplatin,    The Effect of Boric Acid and Borax on Oxidative Stress, Inflammation, ER Stress and Apoptosis in Cisplatin Toxication and Nephrotoxicity Developing as a Result of Toxication
- in-vivo, NA, NA
*ROS↓, decreased inflammation and oxidative stress caused by cisplatin
*Inflam↓,
RenoP↑, boric acid and borax reduced apoptotic damage in kidney tissue,

729- Bor,    Promising potential of boron compounds against Glioblastoma: In Vitro antioxidant, anti-inflammatory and anticancer studies
- in-vitro, GBM, U87MG - in-vivo, Nor, HaCaT
TOS↑,
TumCG↓,
MDA↑,
SOD↑,
Catalase↑,
TAC↓,
GSH↓,
BRAF↑,
MAPK↓,
PTEN↓, BA application was found more favorable because of its inhibitory effect on PIK3CA, PIK3R1, PTEN and RAF1 genes
Raf↓, RAF1
*toxicity↓, We verified the selectivity of the compounds using a normal cell line, HaCaT and found an exact opposite condition after treating HaCaT cells with BA and BX

728- Bor,    Boric Acid and Borax Protect Human Lymphocytes from Oxidative Stress and Genotoxicity Induced by 3-Monochloropropane-1,2-diol
other↓, BA and BX are safe and non-genotoxic under the in vitro conditions and can alleviate cytotoxic, oxidative, and genetic damage induced by 3-MCPD in the human blood cells.

727- Bor,  RSL3,  erastin,    Enhancement of ferroptosis by boric acid and its potential use as chemosensitizer in anticancer chemotherapy
- in-vitro, Liver, HepG2
ROS↑, at high, pharmacological concentrations
GSH↓, BA can increase intracellular ROS,
TBARS↑,
Ferroptosis↑,
ChemoSen↑, These observations suggest that BA could be exploited as a chemo-sensitizer agent in order to overcome cancer drug resistance in selected conditions.

726- Bor,    Redox Mechanisms Underlying the Cytostatic Effects of Boric Acid on Cancer Cells—An Issue Still Open
- Review, NA, NA
NAD↝, high affinity for the ribose moieties of NAD+
SAM-e↝, high affinity for S-adenosylmethione
PSA↓,
IGF-1↓,
Cyc↓, reduction in cyclins A–E
P21↓,
p‑MEK↓,
p‑ERK↓, ERK (P-ERK1/2)
ROS↑, induce oxidative stress by decreasing superoxide dismutase (SOD) and catalase (CAT)
SOD↓,
Catalase↓,
MDA↑,
GSH↓,
IL1↓, IL-1α
IL6↓,
TNF-α↓,
BRAF↝,
MAPK↝,
PTEN↝,
PI3K/Akt↝,
eIF2α↑,
ATF4↑,
ATF6↑,
NRF2↑,
BAX↑,
BID↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Bcl-xL↓,

725- Bor,    Boric acid exert anti-cancer effect in poorly differentiated hepatocellular carcinoma cells via inhibition of AKT signaling pathway
- in-vitro, HCC, NA
tumCV↓, decreased survival
Apoptosis↑,
TumAuto↑,
p‑Akt↓, boric acid might be a promising therapeutic candidate in hepatocellular carcinoma via the inhibition of AKT signaling pathway.

724- Bor,    Does Boric Acid Inhibit Cell Proliferation on MCF-7 and MDA-MB-231 Cells in Monolayer and Spheroid Cultures by Using Apoptosis Pathways?
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
Apoptosis↑,
Casp3↝, expression significantly changed
Casp8↝,
Casp9↝,

723- Bor,    Boric acid suppresses cell proliferation by TNF signaling pathway mediated apoptosis in SW-480 human colon cancer line
- in-vitro, Colon, SW480
Apoptosis↑,
TNF-α↝, he observed apoptotic process was related to the TNF signaling pathway

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: 98

Results for Effect on Cancer/Diseased Cells:
ACSL4↑,1,   Akt↓,1,   p‑Akt↓,1,   angioG↓,1,   AntiCan↑,2,   APAF1↑,1,   Apoptosis↑,16,   AR↓,1,   ATF4↑,5,   ATF6↑,3,   ATM↓,2,   p‑ATM↑,1,   BAX↑,4,   Bcl-2↓,6,   Bcl-xL↓,2,   Beclin-1↑,1,   BID↑,1,   BioAv↑,2,   BRAF↑,1,   BRAF↝,1,   BRCA1↑,1,   BRCA2↑,1,   Ca+2↓,6,   Casp10∅,1,   Casp3↑,10,   Casp3↝,1,   Casp7↑,2,   Casp8↝,1,   Casp8∅,1,   Casp9↑,3,   Casp9↝,1,   Catalase↓,1,   Catalase↑,2,   CD38↑,1,   Cdc42↓,2,   CDH1↑,2,   CDK4∅,1,   CDK6∅,1,   chemoP↑,1,   ChemoSen↑,1,   ChemoSideEff↓,1,   CHOP↓,1,   CHOP↑,1,   cMyc↓,1,   COL1A1↓,3,   Cyc↓,3,   cycD1∅,1,   DHT↑,1,   DNAdam↑,1,   DR4∅,1,   DR5∅,1,   E-cadherin↑,2,   eff↓,1,   eff↑,4,   EGFR↓,1,   eIF2α↑,3,   p‑eIF2α↑,2,   EMT↓,1,   ER Stress↑,2,   ER Stress↝,1,   p‑ERK↓,1,   p‑ERK⇅,1,   FADD∅,1,   Ferroptosis↑,3,   GADD34↑,2,   GCLC↑,1,   Glycolysis↝,1,   GNLY↓,1,   GPx↑,1,   GPx4↓,2,   GranA↓,1,   GranB↓,1,   GRP78/BiP↑,4,   GRP94↑,1,   GSH↓,5,   GutMicro↑,1,   HDAC↓,3,   HDL↓,1,   HIF-1↓,1,   Hif1a↓,2,   HO-1↑,1,   HSP70/HSPA5↓,1,   IFN-γ↓,1,   IGF-1↓,5,   IGF-1↝,1,   IL1↓,2,   IL10↑,1,   IL6↓,2,   IRE1∅,1,   ITGA5↑,3,   ITGB1↑,3,   LAMA5↑,3,   LAMP2↓,1,   LAT↓,1,   LC3II↑,1,   MAPK↓,2,   MAPK↝,1,   MDA↓,1,   MDA↑,4,   p‑MEK↓,1,   miR-126↑,1,   miR-127-5p↑,2,   miR-130a↓,1,   miR-21↓,3,   MMP3↓,1,   MOB1↓,1,   NAD↓,1,   NAD↝,1,   NADHdeh↓,1,   NLRP3↓,1,   NOXA↑,1,   NQO1↑,1,   NRF2↓,1,   NRF2↑,3,   OS↑,1,   OSI↑,1,   other↓,2,   other↑,1,   P21↓,1,   P53↓,1,   P53↑,1,   p‑P53↑,1,   p62↓,1,   p70S6↓,1,   PARP↓,2,   PCBP1↓,1,   PD-1↑,1,   PD-L1↑,1,   Perforin↓,1,   PI3K/Akt↝,1,   PSA↓,7,   PSMB5↓,1,   PTEN↓,1,   PTEN↑,1,   PTEN↝,1,   Rac1↓,1,   radioP↑,1,   RadioS↑,1,   Raf↓,1,   RenoP↑,1,   Rho↓,2,   Risk↓,11,   Risk∅,1,   ROS↑,6,   SA↓,1,   SAM-e↑,1,   SAM-e↝,2,   selectivity↑,3,   serineP↓,2,   sFasL↑,1,   SLC12A5↓,1,   Snail↑,3,   SOD↓,1,   SOD↑,2,   TAC↓,1,   TBARS↑,1,   TNF-α↓,3,   TNF-α↝,1,   TOS↓,1,   TOS↑,2,   TSC2↑,1,   TumAuto↑,2,   TumCCA↑,4,   TumCD↑,1,   TumCG↓,7,   TumCI↓,1,   TumCM/A↑,1,   TumCMig↓,4,   TumCP↓,9,   tumCV↓,1,   TumVol↓,4,   UPR↑,1,   VEGF↓,2,   Vim↓,3,   VitD↑,1,   p‑YAP/TEAD↝,1,   Zeb1↑,3,  
Total Targets: 177

Results for Effect on Normal Cells:
5LO↓,1,   AChE↓,1,   ALAT↓,2,   ALP↓,2,   AMPK↑,2,   angioG↑,1,   antiOx↑,3,   Apoptosis↓,2,   AST↓,2,   ATP↝,1,   Aβ↓,1,   BioAv↑,1,   BMD↑,4,   BMPs↑,1,   Ca+2?,1,   Ca+2↓,1,   Ca+2↝,1,   Calcium↑,2,   cardioP↑,1,   Casp3↓,1,   Catalase↑,4,   CEBPA↓,1,   chemoP↑,1,   ChemoSideEff↓,1,   CHOP↓,1,   cognitive↑,3,   COL1↑,1,   cortisol↑,1,   COX2↓,2,   creat↓,1,   CXCR2↑,1,   Cyt‑c↓,1,   DHT↑,1,   DNAdam↓,1,   Dose↑,1,   Dose↝,1,   eff↓,1,   eff↑,2,   FABP4↓,1,   FASN↓,1,   FGF↑,1,   glucose↓,1,   GLUT4↓,1,   GPx↓,1,   GPx↑,2,   GRP78/BiP↓,1,   GSH↑,3,   Half-Life↑,2,   Half-Life↝,2,   hepatoP↑,3,   HO-1↑,2,   hs-CRP↓,2,   HSP70/HSPA5↑,1,   IL10↑,1,   IL1β↓,2,   IL6↓,4,   IL8↓,1,   Inflam↓,7,   iNOS↓,2,   JAK2↓,2,   Keap1↓,1,   lipid-P↓,3,   Mag↑,2,   MDA↓,6,   memory↑,3,   MIP‑1α↓,1,   MMP↑,3,   MMP2↓,1,   motorD↑,1,   NAD↝,1,   neuroP↑,3,   NF-kB↓,4,   NO↓,2,   NRF2↑,3,   other↑,1,   PGE2↓,1,   PPARγ↓,1,   RenoP↓,1,   RenoP↑,1,   Risk↓,1,   ROS↓,9,   SAM-e↑,1,   selectivity↑,1,   Sema3A/PlexinA1↑,1,   serineP↓,1,   SHBG↓,1,   SOD↑,6,   SREBP1↓,1,   STAT3↓,2,   testos↑,1,   TGF-β↑,1,   TNF-α↓,6,   TNF-α↑,1,   TOS↓,2,   toxicity↓,6,   VEGF↑,1,   VitD↑,4,   α-SMA↑,1,   β-catenin/ZEB1↑,1,  
Total Targets: 99

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:46  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page