BMPs Cancer Research Results
BMPs, Bone morphogenetic protein: Click to Expand ⟱
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BMPs are important cytokines belonging to the Transforming Growth Factor (TGF)-β superfamily. BMP2 is highly overexpressed in human non-small cell lung cancer (NSCLC) and correlates with tumor stage and metastatic burden. BMP-2 level from patients with bone metastasis is significantly higher compared to patients without bone metastasis.
BMPs display significantly higher expression in tumors, which have been used as new biomarkers for the prognosis of cancer patients.
However, some data revealed an opposite role of BMP signaling in tumors. BMP-10 was downregulated in gastric cancer samples. BMP-6 expression was also absent in breast cancer tissues and might suppress breast cancer metastasis.
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Scientific Papers found: Click to Expand⟱
*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.
*chemoPv↑, promising chemopreventive agents
PSA↓,
TGF-β↓, down regulation of the expression of TGF-β and an up-regulation of the bone morphogenic protein BMP-2 as a result of curcumin feeding
BMPs↑, BMP2,7
TumMeta↓, Curcumin Inhibits Prostate Cancer Bone Metastasis
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*P-gp↓, reduction in the expression of defective proteins like P-glycoproteins, inhibition of oxidative stress, suppression of pro-inflammatory cytokines (TNF-α, IL-10 and IL-6),
*ROS↓,
*TNF-α↓,
*IL10↓,
*IL6↓,
eIF2α↑, Bcl-2, phosphorylated eIF2α, CHOP,GRP78, Bax, cleaved caspase-9 and phosphorylated PERK
CHOP↑,
GRP78/BiP↑,
BAX↑,
cl‑Casp9↑,
p‑PERK↑,
ER Stress↑, endoplasmic reticulum stress and proteins in apoptosis in 95-D and A549 cells
Apoptosis↑,
MMPs↓, decrease in levels of matrix metal-mloproteinases, P-glycoprotein expression, the formation of mammosphere, H3K27 methyltransferase, c-FLIP, level of CXCR4 receptor,pluripotency-factors, Twist-1, class I histone deacetylases, steroid receptor co
cFLIP↓,
CXCR4↓,
Twist↓,
HDAC↓,
BMPs↑, enhancement in Bax protein, and (BMP7), as well as interference with an activator of transcription 3 (STAT3), (mTOR), (EGFR), (NF-kB) and Shh
p‑STAT3↓, secreased the phosphorylation of STAT3
mTOR↓,
EGFR↓,
NF-kB↓,
Shh↓,
VEGF↓, induce apoptosis, and regulate the vascular endothelial growth factor-A expression (VEGF-A)
tumCV↓, human glioma cell lines (U251 and U-87 MG) through inhibition of colony formation, glioma cell viability, cell migration, invasion, suppression of ERK and AKT signalling cascades, apoptosis induction, and reduction of Bcl-2 expression.
TumCMig↓,
TumCI↓,
ERK↓,
Akt↓,
Bcl-2↓,
Nestin↓, increased the Bax expression, lowered the CD133, EGFR, and Nesti
CD133↓,
p‑cMET↑, HKL through the downregulating the phosphorylation of c-Met phosphorylation and stimulation of Ras,
RAS↑,
chemoP↑, Cheng and coworker determined the chemopreventive role of HKL against the proliferation of renal cell carcinoma (RCC) 786â0 cells
through multiple mechanism
*NRF2↑, , HKL also effectively activate the Nrf2/ARE pathway and reverse this pancreatic dysfunction in in vivo
and in vitro model
*NADPH↓, (HUVECs) such as inhibition of NADPH oxidase activity, suppression of p22 (phox) protein expression, Rac-1 phosphorylation, reactive oxygen species production, inhibition of degradation of Ikappa-B-alpha, and suppression of activity of of NF-kB
*p‑Rac1↓,
*ROS↓,
*IKKα↑,
*NF-kB↓,
*COX2↓, Furthermore, HKL treatment the inhibited cyclooxygenase (COX-2) upregulation, reduces prostaglandin E2 production, enhanced caspase-3 activity reduction
*PGE2↓,
*Casp3↓,
*hepatoP↑, compound also displayed hepatoprotective action against oxidative injury in tert-butyl hydroperoxide (t-BHP)-injured AML12
liver cells in in vitro model
*antiOx↑, compound reduces the level of acetylation on SOD2 to stimulate its antioxidative action, which results in reduced reactive oxygen
species aggregation in AML12 cells
*GSH↑, HKL prevents oxidative damage induced by H2O2 via elevating antioxidant enzymes levels which includes glutathione and catalase and promotes translocation and activation transcription factor Nrf2
*Catalase↑,
*RenoP↑, imilarly, the compound protects renal reperfusion/i-schemia injury (IRI) in adult male albino Wistar rats via reducing theactivities of serum alkaline phosphatase (ALP), aspartate aminotrans-
ferase (AST) and alanine aminotransferase (ALT)
*ALP↓,
*AST↓,
*ALAT↓,
*neuroP↑, Several reports and works have shown that HKL displays some neuroprotective properties
*cardioP↑, Cardioprotection
*HO-1↑, the expression level of heme oxygenase-1 (HO-1)was remarkably up-regulated and miR-218-5p was significantly down-regulated in septic mice treated with HKL
*Inflam↓, anti-inflammatory action of
HKL at dose of 10 mg/kg in the muscle layer of mice
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*BioAv↓, HNK showed poor aqueous solubility due to phenolic hydroxyl groups forming intramolecular hydrogen bonds and
poor solubility in water (
*neuroP↑, HNK has the accessibility to reach the neuronal tissue by crossing the BBB and showing neuroprotective effects
*BBB↑,
*ROS↓, fig 2
*Keap1↑,
*NRF2↑,
*Casp3↓,
*SIRT3↑,
*Rho↓,
*ERK↓,
*NF-kB↓,
angioG↓,
RAS↓,
PI3K↓,
Akt↓,
mTOR↓,
*memory↑, oral administration of HNK (1 mg/kg) in senescence-accelerated mice prevents age-related memory and learning deficits
*Aβ↓, in Alzheimer’s disease, HNK significantly reduces neurotoxicity of aggregated Ab
*PPARγ↑, Furthermore, the expression of PPARc and PGC1a was increased by HNK, suggesting its beneficial impact on energy metabolism
*PGC-1α↑,
NF-kB↓, activation of NFjB was suppressed by HNK via suppression of nuclear translocation and phosphorylation of the p65 subunit and further instigated apoptosis by enhancing TNF-a
Hif1a↓, HNK has anti-oxidative properties and can downregulate the HIF-1a protein, inhibiting hypoxia-
related signaling pathways
VEGF↓, renal cancer, via decreasing the vascular endothelial growth factor (VEGF) and heme-oxygenase-1 (HO-1)
HO-1↓,
FOXM1↓, HNK interaction with the FOXM1 oncogenic transcription factor inhibits cancer cells
p27↑, HNK treatment upregulates the expression of CDK inhibitor p27 and p21, whereas it downregulates the expression of CDK2/4/6 and cyclin D1/2
P21↑,
CDK2↓,
CDK4↓,
CDK6↓,
cycD1/CCND1↓,
Twist↓, HNK averted the invasion of urinary bladder cancer cells
by downregulating the steroid receptor coactivator, Twist1
and Matrix metalloproteinase-2
MMP2↓,
Rho↑, By activating the RhoA, ROCK and MLC signaling, HNK inhibits the migration of highly metastatic renal cell carcinoma
ROCK1↑,
TumCMig↓,
cFLIP↓, HNK can be used to suppress c-FLIP, the apoptosis inhibitor.
BMPs↑, HNK treatment increases the expression of BMP7 protein
OCR↑, HNK might increase the oxygen consumption rate while decreasing the extracellular acidification rate in breast cancer
cells.
ECAR↓,
*AntiAg↑, It also suppresses the platelet aggregation
*cardioP↑, HNK is an attractive cardioprotective agent because of its strong antioxidative properties
*antiOx↑,
*ROS↓, HNK treatment reduced cellular ROS production and decreased mitochondrial damage in
neonatal rat cardiomyocytes exposed to hypoxia/reoxygenation
P-gp↓, The expres-
sion of P-gp at mRNA and protein levels is reduced in HNK
treatment on human MDR and MCF-7/ADR breast cancer cell
lines
*other↑, The expression of placental growth factor (PlGF) was significantly higher in the PEMF-treated group compared to the expression level before PEMF treatment.
*BDNF↑, Other factors trended higher following active PEMF treatment including BDNF and BMP-7 and -5.
*BMPs↑,
*BMD↑, PEMF accelerated bone regeneration, resulting in increased BV and BMD in groups that received 0, 2.5, and 5 μg rhBMP-2.
Calcium↑,
MMP1↑, 2.8x
MMP3↑, 2.1x
BMPs↑, BMP-2 increase untill after day 9
xCT↓, Sulfasalazine (SSZ), a drug used to treat rheumatoid arthritis, suppresses xCT expression in cancer cells.
GSH↓, this treatment decreased the intracellular glutathione concentration.
BMPs↑, significantly increased alizarin red staining and its quantification, as well as the concentration-dependent osteogenic differentiation markers (BMP1 and SPP) mRNA expression.
Diff↑, SSZ treatment of CADSCs increased the efficiency of osteogenic differentiation induction in vitro.
Showing Research Papers: 1 to 7 of 7
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↓, 1, HO-1↓, 1, xCT↓, 1,
Mitochondria & Bioenergetics ⓘ
OCR↑, 1,
Core Metabolism/Glycolysis ⓘ
ECAR↓, 1,
Cell Death ⓘ
Akt↓, 2, Apoptosis↑, 2, BAX↑, 1, Bcl-2↓, 1, cl‑Casp9↑, 1, cFLIP↓, 2, p27↑, 1,
Transcription & Epigenetics ⓘ
tumCV↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, eIF2α↑, 1, ER Stress↑, 1, GRP78/BiP↑, 1, p‑PERK↑, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 1, Cyc↓, 1, cycD1/CCND1↓, 1, P21↑, 1,
Proliferation, Differentiation & Cell State ⓘ
CD133↓, 1, p‑cMET↑, 1, Diff↑, 1, ERK↓, 1, FOXM1↓, 1, HDAC↓, 2, IGF-1↓, 1, mTOR↓, 2, Nestin↓, 1, PI3K↓, 1, RAS↓, 1, RAS↑, 1, Shh↓, 1, p‑STAT3↓, 1,
Migration ⓘ
MMP1↑, 1, MMP2↓, 1, MMP3↑, 1, MMPs↓, 1, Rho↑, 1, ROCK1↑, 1, TGF-β↓, 1, TumCI↓, 1, TumCMig↓, 3, TumMeta↓, 1, Twist↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EGFR↓, 1, HIF-1↓, 1, Hif1a↓, 1, VEGF↓, 2,
Barriers & Transport ⓘ
P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
CXCR4↓, 1, NF-kB↓, 2, PSA↓, 2,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 1,
Clinical Biomarkers ⓘ
BMPs↑, 5, Calcium↑, 1, EGFR↓, 1, FOXM1↓, 1, PSA↓, 2,
Functional Outcomes ⓘ
AntiCan↑, 1, chemoP↑, 1, Risk↓, 1, TumVol↓, 1,
Total Targets: 67
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, Catalase↑, 2, GPx↑, 1, GSH↑, 1, HO-1↑, 1, Keap1↑, 1, NRF2↑, 2, ROS↓, 4, SAM-e↑, 1, SIRT3↑, 1, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↝, 1, PGC-1α↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, NAD↝, 1, NADPH↓, 1, PPARγ↑, 1,
Cell Death ⓘ
Casp3↓, 2,
Transcription & Epigenetics ⓘ
other↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↓, 1,
Migration ⓘ
AntiAg↑, 1, Ca+2↝, 1, p‑Rac1↓, 1, Rho↓, 1, serineP↓, 1,
Barriers & Transport ⓘ
BBB↑, 1, P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IKKα↑, 1, IL10↓, 1, IL6↓, 1, Inflam↓, 2, NF-kB↓, 2, PGE2↓, 1, TNF-α↓, 2, VitD↑, 1,
Synaptic & Neurotransmission ⓘ
BDNF↑, 1,
Protein Aggregation ⓘ
Aβ↓, 1,
Hormonal & Nuclear Receptors ⓘ
testos↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, Dose↑, 1, Dose↝, 1, eff↑, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, ALP↓, 1, AST↓, 1, BMD↑, 2, BMPs↑, 2, Calcium↑, 1, hs-CRP↓, 1, IL6↓, 1, Mag↑, 1, VitD↑, 1,
Functional Outcomes ⓘ
cardioP↑, 2, chemoP↑, 1, chemoPv↑, 1, ChemoSideEff↓, 1, cognitive↑, 1, hepatoP↑, 1, memory↑, 2, neuroP↑, 3, RenoP↑, 1, Risk↓, 1,
Total Targets: 64
Scientific Paper Hit Count for: BMPs, Bone morphogenetic protein
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
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