TSP-1 Cancer Research Results
TSP-1, Thrombospondin-1: Click to Expand ⟱
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(TSP-1) is the first reported endogenous anti-angiogenic factor that can inhibit angiogenesis and tumorigenesis.
Thrombospondin-1 (TSP-1) is a glycoprotein that plays a significant role in various biological processes, including cell adhesion, migration, and angiogenesis. It is part of the thrombospondin family of proteins and is known for its ability to regulate the formation of new blood vessels (angiogenesis) and modulate the immune response.
TSP-1 is often considered a tumor suppressor because it can inhibit angiogenesis by binding to and activating certain receptors on endothelial cells, leading to reduced blood vessel formation. This can limit the supply of nutrients and oxygen to tumors, potentially inhibiting their growth.
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Scientific Papers found: Click to Expand⟱
Apoptosis↑,
TumCCA↓, CAPE (1-80 uM) can stimulate apoptosis and cell cycle arrest (G1 phase
TumCMig↓,
TumMeta↓,
ChemoSen↑,
eff↑, Nanoparticles promote therapeutic effect of CA and CAPE in reducing cancer cell malignancy.
eff↑, improve capacity of CA and CAPE in cancer suppression, it has been co-administered with other anti-tumor compounds such as gallic acid
eff↓, Currently, solvent extraction is utilized by methanol and ethyl acetate
combination at high temperatures. However, a low amount of CA is
yielded via this pathway
eff↝, Decyl CA (DCA) is a
novel derivative of CA but its role in affecting colorectal cancer has not
been completely understood.
Dose∅, The CAPE administration (0-60 uM) induces both
autophagy and apoptosis in C6 glioma cells.
AMPK↑, CAPE induces autophagy via AMPK upregulation.
p62↓, CAPE can induce autophagy via p62 down-regulation and LC3-II upregulation
LC3II↑,
Ca+2↑, CA (0-1000 uM) enhances Ca2+ accumulation in cells in a concentration-dependent manner
Bax:Bcl2↑, CA can promote Bax/Bcl-2 ratio i
CDK4↑, The administration of CAPE (1–80 μM)
can stimulate apoptosis and cell cycle arrest (G1 phase) via upregulation of Bax, CDK4, CDK6 and Rb
CDK6↑,
RB1↑,
EMT↓, CAPE has demonstrated high potential in inhibiting EMT in nasopharyngeal caner via enhancing E-cadherin levels, and reducing vimentin and β-catenin levels.
E-cadherin↑,
Vim↓,
β-catenin/ZEB1↓,
NF-kB↓,
angioG↑, CAPE (0.01-1ug/ml) inhibited angiogenesis via VEGF down-regulation
VEGF↓,
TSP-1↑, and furthermore, CAPE is capable of increasing TSP-1 levels
MMP9↓, CAPE was found to reduce MMP-9 expression
MMP2↓, CAPE can also down-regulate MMP-2
ChemoSen↑, role of CA and its derivatives in enhancing therapy sensitivity of cancer cells.
eff↑, CA administration (100 uM) alone or its combination with metformin (10 mM) can induce AMPK signaling
ROS↑, CA can promote ROS levels to induce cell death in human squamous cell carcinoma
CSCs↓, CA can reduce self-renewal capacity of CSCs and their migratory ability in vitro and in vivo.
Fas↑, CAPE (0-100 uM) is capable of inducing Fas signaling to promote p53 expression, leading to apoptotic cell death via Bax and caspase activation
P53↑,
BAX↑,
Casp↑,
β-catenin/ZEB1↓, anti-tumor activity of CAPE is mediated via reducing β-catenin levels
NDRG1↑, CAPE (30 uM) can promote NDRG1 expression via MAPK activation and down-regulation of STAT3
STAT3↓,
MAPK↑, CAPE stimulates mitogen-activated protein kinase (MAPK) and ERK
ERK↑,
eff↑, Res, thymoquinone and CAPE mediate lung tumor cell death via Bax
upregulation and Bcl-2 down-regulation.
eff↑, co-administration of CA (100 μM) and
metformin (10 mM) is of interest in cervical squamous cell carcinoma
therapy.
eff↑, in addition to CA, propolis contains other agents such as chrysin, p-coumaric acid and ferulic acid that are beneficial in tumor suppression.
toxicity↓, Four clinical trials and two case reports evaluating metronomic chemotherapy for HCC indicate it to be a safe and potentially useful treatment for HCC
toxicity↓, usually associated with much less severe acute toxicities compared to conventional MTD chemotherapy
eff↝, So, recently, metronomic chemotherapy has been investigated in pediatric oncology
angioG↓, The main antitumor effects caused by metronomic chemotherapy are thought to be inhibition of tumor-associated vascular development and stimulation of immunity rather than direct cytotoxic effects on tumor cells
CSCs↓, However, intriguingly, some recent reports have implicated direct targeting of cancer stem cells as a possible mechanism of metronomic cyclophosphamide
TSP-1↑, Bocci et al. [83,84] reported that protracted exposure of endothelial cells in vitro to low concentrations of various anticancer chemotherapeutic agents and ceramide analog caused marked induction of gene and protein expression of TSP-1.
Hif1a↓, Continuous administration of low-doseα topotecan was reported to decrease the expression of HIF-1 [34], VEGF, and SDF-1
VEGF↓,
eff↑, About 80% of the trials have reported positive efficacy of metronomic chemotherapy.
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in-vitro, |
HCC, |
HUH7 |
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in-vivo, |
HCC, |
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TumCG↓, Metronomic S-1 significantly inhibited tumor growth, which was enhanced by combination with vandetanib.
toxicity↓, With respect to toxicities, MTD S-1 caused severe body weight loss and myelosuppression, whereas metronomic S-1 did not cause any overt toxicities.
OS↑, Moreover, metronomic S-1 or metronomic S-1 with vandetanib prolonged survival, the latter treatment providing the greatest benefit.
TSP-1↑, whereas the expression of thrombospondin-1 was upregulated by metronomic S-1 and metronomic S-1 with vandetanib.
Dose↓, The IC50 levels for the MTD and metronomic schedule for Huh-7 cells were 3.84 and 0.77 µM, respectively
Dose↓, hepatoma cell lines, the metronomic schedule inhibited cell proliferation at approximately 1/2 to 1/4 concentrations of 5-FU compared with MTD schedule
TSP-1↑, protein + mRNA
angioG↓, quercetin can effectively inhibit angiogenesis through TSP-1 upregulation to antagonize human prostate cancer PC-3 cell growth in vitro and in vivo.
TumCMig↓, After treated with quercetin at 25, 50 and 100 µM for 24 h, the migration, invasion and tube formation were also inhibited
TumCI↓,
ROS↑, decided by the availability of intracellular reduced glutathione (GSH),
GSH↓, extended exposure with high concentration of quercetin causes a substantial decline in GSH levels
Ca+2↝,
MMP↓,
Casp3↑, activation of caspase-3, -8, and -9
Casp8↑,
Casp9↑,
other↓, when p53 is inhibited, cancer cells become vulnerable to quercetin-induced apoptosis
*ROS↓, Quercetin (QC), a plant-derived bioflavonoid, is known for its ROS scavenging properties and was recently discovered to have various antitumor properties in a variety of solid tumors.
*NRF2↑, Moreover, the therapeutic efficacy of QC has also been defined in rat models through the activation of Nrf-2/HO-1 against high glucose-induced damage
HO-1↑,
TumCCA↑, QC increases cell cycle arrest via regulating p21WAF1, cyclin B, and p27KIP1
Inflam↓, QC-mediated anti-inflammatory and anti-apoptotic properties play a key role in cancer prevention by modulating the TLR-2 (toll-like receptor-2) and JAK-2/STAT-3 pathways and significantly inhibit STAT-3 tyrosine phosphorylation within inflammatory ce
STAT3↓,
DR5↑, several studies showed that QC upregulated the death receptor (DR)
P450↓, it hinders the activity of cytochrome P450 (CYP) enzymes in hepatocytes
MMPs↓, QC has also been shown to suppress metastatic protein expression such as MMPs (matrix metalloproteases)
IFN-γ↓, QC is its ability to inhibit inflammatory mediators including IFN-γ, IL-6, COX-2, IL-8, iNOS, TNF-α,
IL6↓,
COX2↓,
IL8↓,
iNOS↓,
TNF-α↓,
cl‑PARP↑, Induced caspase-8, caspase-9, and caspase-3 activation, PARP cleavage, mitochondrial membrane depolarization,
Apoptosis↑, increased apoptosis and p53 expression
P53↑,
Sp1/3/4↓, HT-29 colon cancer cells: decreased the expression of Sp1, Sp3, Sp4 mrna, and survivin,
survivin↓,
TRAILR↑, H460 Increased the expression of TRAILR, caspase-10, DFF45, TNFR 1, FAS, and decreased the expression of NF-κb, ikkα
Casp10↑,
DFF45↑,
TNFR 1↑,
Fas↑,
NF-kB↓,
IKKα↓,
cycD1/CCND1↓, SKOV3 Reduction in cyclin D1 level
Bcl-2↓, MCF-7, HCC1937, SK-Br3, 4T1, MDA-MB-231 Decreased Bcl-2 expression, increasedBax expression, inhibition of PI3K-Akt pathway
BAX↑,
PI3K↓,
Akt↓,
E-cadherin↓, MDA-MB-231 Induced the expression of E-cadherin and downregulated vimentin levels, modulation of β-catenin target genes such as cyclin D1 and c-Myc
Vim↓,
β-catenin/ZEB1↓,
cMyc↓,
EMT↓, MCF-7 Suppressed the epithelial–mesenchymal transition process, upregulated E-cadherin expression, downregulated vimentin and MMP-2 expression, decreased Notch1 expression
MMP2↓,
NOTCH1↓,
MMP7↓, PANC-1, PATU-8988 Decreased the secretion of MMP and MMP7, blocked the STAT3 signaling pathway
angioG↓, PC-3, HUVECs Reduced angiogenesis, increased TSP-1 protein and mrna expression
TSP-1↑,
CSCs↓, PC-3 and LNCaP cells Activated capase-3/7 and inhibit the expression of Bcl-2, surviving and XIAP in CSCs.
XIAP↓,
Snail↓, inhibiting the expression of vimentin, slug, snail and nuclear β-catenin, and the activity of LEF-1/TCF responsive reporter
Slug↓,
LEF1↓,
P-gp↓, MCF-7 and MCF-7/dox cell lines Downregulation of P-gp expression
EGFR↓, MCF-7 and MDA-MB-231 cells Suppressed EGFR signaling and inhibited PI3K/Akt/mTOR/GSK-3β
GSK‐3β↓,
mTOR↓,
RAGE↓, IA Paca-2, BxPC3, AsPC-1, HPAC and PANC1 Silencing RAGE expression
HSP27↓, Breast cancer In vivo NOD/SCID mice Inhibited the overexpression of Hsp27
VEGF↓, QC significantly reversed an elevation in profibrotic markers (VEGF, IL-6, TGF, COL-1, and COL-3)
TGF-β↓,
COL1↓,
COL3A1↓,
*Inflam↓, quercetin is known for its anti-inflammatory, antioxidant, and anticancer properties.
*antiOx↑,
*AntiCan↑,
Casp3↓, Quercetin increases apoptosis and autophagy in cancer by activating caspase-3, inhibiting the phosphorylation of Akt, mTOR, and ERK, lessening β-catenin, and stabilizing the stabilization of HIF-1α.
p‑Akt↓,
p‑mTOR↓,
p‑ERK↓,
β-catenin/ZEB1↓,
Hif1a↓,
AntiAg↓, Quercetin have revealed an anti-tumor effect by reducing development of blood vessels. I
VEGFR2↓, decrease tumor growth through targeting VEGFR-2-mediated angiogenesis pathway and suppressing the downstream regulatory component AKT in prostate and breast malignancies.
EMT↓, effects of quercetin on inhibition of EMT, angiogenesis, and invasiveness through the epidermal growth factor receptor (EGFR)/VEGFR-2-mediated pathway in breast cancer
EGFR↓,
MMP2↓, MMP2 and MMP9 are two remarkable compounds in metastatic breast cancer (28–30). quercetin on breast cancer cell lines (MDA-MB-231) and showed that after treatment with this flavonoid, the expression of these two proteinases decreased
MMP↓,
TumMeta↓, head and neck (HNSCC), the inhibitory effect of quercetin on the migration of tumor cells has been shown by regulating the expression of MMPs
MMPs↓,
Akt↓, quercetin by inhibiting the Akt activation pathway dependent on Snail, diminishing the expression of N-cadherin, vimentin, and ADAM9 and raising the expression of E-cadherin and proteins
Snail↓,
N-cadherin↓,
Vim↓,
E-cadherin↑,
STAT3↓, inhibiting STAT3 signaling
TGF-β↓, reducing the expression of TGF-β caused by vimentin and N-cadherin, Twist, Snail, and Slug and increasing the expression of E-cadherin in PC-3 cells.
ROS↓, quercetin exerted an anti-proliferative role on HCC cells by lessening intracellular ROS independently of p53 expression
P53↑, increasing the expression of p53 and BAX in hepatocellular carcinoma (HepG2) cell lines through the reduction of PKC, PI3K, and cyclooxygenase (COX-2)
BAX↑,
PKCδ↓,
PI3K↓,
COX2↓,
cFLIP↓, quercetin by inhibiting PI3K/AKT/mTOR and STAT3 pathways, decreasing the expression of cellular proteins such as c-FLIP, cyclin D1, and c-Myc, as well as reducing the production of IL-6 and IL-10 cytokines, leads to the death of PEL cells
cycD1/CCND1↓,
cMyc↓,
IL6↓,
IL10↓,
Cyt‑c↑, In addition, quercetin induced c-cytochrome-dependent apoptosis and caspase-3 almost exclusively in the HSB2 cell line
TumCCA↑, Exposure of K562 cells to quercetin also significantly raised the cells in the G2/M phase, which reached a maximum peak in 24 hours
DNMTs↓, pathway through DNA demethylation activity, histone deacetylase (HDAC) repression, and H3ac and H4ac enrichment
HDAC↓,
ac‑H3↑,
ac‑H4↑,
Diablo↑, SMAC/DIABLO exhibited activation
Casp3↑, enhanced levels of activated caspase 3, cleaved caspase 9, and PARP1
Casp9↑,
PARP1↑,
eff↑, green tea and quercetin as monotherapy caused the reduction of levels of anti-apoptotic proteins, CDK6, CDK2, CYCLIN D/E/A, BCL-2, BCL-XL, and MCL-1 and an increase in expression of BAX.
PTEN↑, Quercetin upregulates the level of PTEN as a tumor suppressor, which inhibits AKT signaling
VEGF↓, Quercetin had anti-inflammatory and anti-angiogenesis effects, decreasing VGEF-A, NO, iNOS, and COX-2 levels
NO↓,
iNOS↓,
ChemoSen↑, quercetin and chemotherapy can potentiate their effect on the malignant cell
eff↑, combination with hyperthermia, Shen et al. Quercetin is a method used in cancer treatment by heating, and it was found to reduce Doxorubicin hydrochloride resistance in leukemia cell line K562
eff↑, treatment with ellagic acid, luteolin, and curcumin alone showed excellent anticancer effects.
eff↑, co-treatment with quercetin and curcumin led to a reduction of mitochondrial membrane integrity, promotion of cytochrome C release, and apoptosis induction in CML cells
uPA↓, A-549 cells were shown to have reduced mRNA expressions of urokinase plasminogen activator (uPA), Upar, protein expression of CXCR-4, CXCL-12, SDF-1 when quercetin was applied at 20 and 40 mM/ml by real-time PCR.
CXCR4↓,
CXCL12↓,
CLDN2↓, A-549 cells, indicated that quercetin could reduce mRNA and protein expression of Claudin-2 in A-549 cell lines without involving Akt and ERK1/2,
CDK6↓, CDK6, which supports the growth and viability of various cancer cells, was hampered by the dose-dependent manner of quercetin (IC50 dose of QR for A-549 cells is 52.35 ± 2.44 μM).
MMP9↓, quercetin up-regulated the rates of G1 phase cell cycle and cellular apoptotic in both examined cell lines compared with the control group, while it declined the expressions of the PI3K, AKT, MMP-2, and MMP-9 proteins
TSP-1↑, quercetin increased TSP-1 mRNA and protein expression to inhibit angiogenesis,
Ki-67↓, significant reductions in Ki67 and PCNA proliferation markers and cell survival markers in response to quercetin and/or resveratrol.
PCNA↓,
ROS↑, Also, quercetin effectively causes intracellular ROS production and ER stress
ER Stress↑,
FAK↓, Quercetin can inhibit HGF-induced melanoma cell migration by inhibiting the activation of c-Met and its downstream Gabl, FAK and PAK [84]
TumCCA↑, stimulation of cell cycle arrest at the G1 stage
p‑pRB↓, mediated through regulation of p21 CDK inhibitor and suppression of pRb phosphorylation resulting in E2F1 sequestering.
CDK2↑, low dose of quercetin has brought minor DNA injury and Chk2 induction
CycB/CCNB1↓, quercetin has a role in the reduction of cyclin B1 and CDK1 levels,
CDK1↓,
EMT↓, quercetin suppresses epithelial to mesenchymal transition (EMT) and cell proliferation through modulation of Sonic Hedgehog signaling pathway
PI3K↓, quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
MAPK↓,
Wnt↓,
ROS↑, colorectal cancer, quercetin has been shown to suppress carcinogenesis through various mechanisms including affecting cell proliferation, production of reactive oxygen species and expression of miR-21
miR-21↑,
Akt↓, Figure 1 anti-cancer mechanisms
NF-kB↓,
FasL↑,
Bak↑,
BAX↑,
Bcl-2↓,
Casp3↓,
Casp9↑,
P53↑,
p38↑,
MAPK↑,
Cyt‑c↑,
PARP↓,
CHOP↑,
ROS↓,
LDH↑,
GRP78/BiP↑,
ERK↑,
MDA↓,
SOD↑,
GSH↑,
NRF2↑,
VEGF↓,
PDGF↓,
EGF↓,
FGF↓,
TNF-α↓,
TGF-β↓,
VEGFR2↓,
EGFR↓,
FGFR1↓,
mTOR↓,
cMyc↓,
MMPs↓,
LC3B-II↑,
Beclin-1↑,
IL1β↓,
CRP↓,
IL10↓,
COX2↓,
IL6↓,
TLR4↓,
Shh↓,
HER2/EBBR2↓,
NOTCH↓,
DR5↑, quercetin has enhanced DR5 expression in prostate cancer cells
HSP70/HSPA5↓, Quercetin has also suppressed the upsurge of hsp70 expression in prostate cancer cells following heat treatment and enhanced the quantity of subG1 cells
CSCs↓, Quercetin could also suppress cancer stem cell attributes and metastatic aptitude of isolated prostate cancer cells through modulating JNK signaling pathway
angioG↓, Quercetin inhibits angiogenesis-mediated of human prostate cancer cells through negatively modulating angiogenic factors (TGF-β, VEGF, PDGF, EGF, bFGF, Ang-1, Ang-2, MMP-2, and MMP-9)
MMP2↓,
MMP9↓,
IGFBP3↑, Quercetin via increasing the level of IGFBP-3 could induce apoptosis in PC-3 cells
uPA↓, Quercetin through decreasing uPA and uPAR expression and suppressing cell survival protein and Ras/Raf signaling molecules could decrease prostate cancer progression
uPAR↓,
RAS↓,
Raf↓,
TSP-1↑, Quercetin through TSP-1 enhancement could effectively inhibit angiogenesis
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, GSH↑, 1, HO-1↑, 1, MDA↓, 1, NRF2↑, 1, ROS↓, 2, ROS↑, 4, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
EGF↓, 1, FGFR1↓, 1, MMP↓, 2, Raf↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, cMyc↓, 3, LDH↑, 1,
Cell Death ⓘ
Akt↓, 3, p‑Akt↓, 1, Apoptosis↑, 2, Bak↑, 1, BAX↑, 4, Bax:Bcl2↑, 1, Bcl-2↓, 2, Casp↑, 1, Casp10↑, 1, Casp3↓, 2, Casp3↑, 2, Casp8↑, 1, Casp9↑, 3, cFLIP↓, 1, Cyt‑c↑, 2, Diablo↑, 1, DR5↑, 2, Fas↑, 2, FasL↑, 1, iNOS↓, 2, MAPK↓, 1, MAPK↑, 2, p38↑, 1, survivin↓, 1, TNFR 1↑, 1, TRAILR↑, 1,
Kinase & Signal Transduction ⓘ
HER2/EBBR2↓, 1, Sp1/3/4↓, 1,
Transcription & Epigenetics ⓘ
ac‑H3↑, 1, ac‑H4↑, 1, miR-21↑, 1, other↓, 1, p‑pRB↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 1, GRP78/BiP↑, 1, HSP27↓, 1, HSP70/HSPA5↓, 1,
Autophagy & Lysosomes ⓘ
Beclin-1↑, 1, LC3B-II↑, 1, LC3II↑, 1, p62↓, 1,
DNA Damage & Repair ⓘ
DFF45↑, 1, DNMTs↓, 1, P53↑, 4, PARP↓, 1, cl‑PARP↑, 1, PARP1↑, 1, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK2↑, 1, CDK4↑, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 2, RB1↑, 1, TumCCA↓, 1, TumCCA↑, 3,
Proliferation, Differentiation & Cell State ⓘ
CSCs↓, 4, EMT↓, 4, ERK↑, 2, p‑ERK↓, 1, FGF↓, 1, GSK‐3β↓, 1, HDAC↓, 1, IGFBP3↑, 1, mTOR↓, 2, p‑mTOR↓, 1, NOTCH↓, 1, NOTCH1↓, 1, PI3K↓, 3, PTEN↑, 1, RAS↓, 1, Shh↓, 1, STAT3↓, 3, TumCG↓, 1, Wnt↓, 1,
Migration ⓘ
AntiAg↓, 1, Ca+2↑, 1, Ca+2↝, 1, CLDN2↓, 1, COL1↓, 1, COL3A1↓, 1, CXCL12↓, 1, E-cadherin↓, 1, E-cadherin↑, 2, FAK↓, 1, Ki-67↓, 1, LEF1↓, 1, MMP2↓, 4, MMP7↓, 1, MMP9↓, 3, MMPs↓, 3, N-cadherin↓, 1, PDGF↓, 1, PKCδ↓, 1, RAGE↓, 1, Slug↓, 1, Snail↓, 2, TGF-β↓, 3, TSP-1↑, 7, TumCI↓, 1, TumCMig↓, 2, TumMeta↓, 2, uPA↓, 2, uPAR↓, 1, Vim↓, 3, β-catenin/ZEB1↓, 4,
Angiogenesis & Vasculature ⓘ
angioG↓, 4, angioG↑, 1, EGFR↓, 3, Hif1a↓, 2, NO↓, 1, VEGF↓, 5, VEGFR2↓, 2,
Barriers & Transport ⓘ
P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 3, CRP↓, 1, CXCR4↓, 1, IFN-γ↓, 1, IKKα↓, 1, IL10↓, 2, IL1β↓, 1, IL6↓, 3, IL8↓, 1, Inflam↓, 1, NF-kB↓, 3, TLR4↓, 1, TNF-α↓, 2,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 1, CDK6↑, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 3, Dose↓, 2, Dose∅, 1, eff↓, 1, eff↑, 11, eff↝, 2, P450↓, 1,
Clinical Biomarkers ⓘ
CRP↓, 1, EGFR↓, 3, HER2/EBBR2↓, 1, IL6↓, 3, Ki-67↓, 1, LDH↑, 1, RAGE↓, 1,
Functional Outcomes ⓘ
NDRG1↑, 1, OS↑, 1, toxicity↓, 3,
Total Targets: 163
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, NRF2↑, 1, ROS↓, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1,
Total Targets: 5
Scientific Paper Hit Count for: TSP-1, Thrombospondin-1
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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