miR-21 Cancer Research Results
miR-21, miR-21: Click to Expand ⟱
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miR-21 is often considered an oncogenic microRNA because its overexpression is frequently observed in many cancers. It can promote tumor growth and progression by targeting and downregulating tumor suppressor genes.
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
Melanoma, |
U266 |
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ROS↑,
TumCCA↑, G2/M phase arrest
Apoptosis↑,
miR-21↓,
Bcl-2↓,
NF-kB↓, 80 μmol/L
Set9↑, 2 fold
chemoPv↑, reviews about cancer chemopreventive role of betulinic acid against wide variety of cancers [18,19,20,21].
p‑STAT3↓, betulinic acid reduced the levels of p-STAT3 in tumor tissues derived from KB cells
JAK1↓, Betulinic acid exerted inhibitory effects on the constitutive phosphorylation of JAK1 and JAK2
JAK2↓,
VEGF↓, betulinic acid mediated inhibition of VEGF
EGFR↓, evaluation of betulinic acid as a next-generation EGFR inhibitor
Cyt‑c↑, release of SMAC/DIABLO and cytochrome c from mitochondria in SHEP neuroblastoma cells
Diablo↑,
AMPK↑, Betulinic acid induced activation of AMPK and consequently reduced the activation of mTOR.
mTOR↓,
Sp1/3/4↓, Betulinic acid significantly reduced the quantities of Sp1, Sp3 and Sp4 in the tissues of the tumors derived from RKO cells
DNAdam↑, Betulinic acid efficiently triggered DNA damage (γH2AX) and apoptosis (caspase-3 and p53 phosphorylation) in temozolomide-sensitive and temozolomide-resistant glioblastoma cells.
Gli1↓, Betulinic acid effectively reduced GLI1, GLI2 and PTCH1 in RMS-13 cells.
GLI2↓,
PTCH1↓,
MMP2↓, betulinic acid exerted inhibitory effects on MMP-2 and MMP-9 in HepG2 cells.
MMP9↓,
miR-21↓, Collectively, p53 increased miR-21 levels and inhibited SOD2 levels, leading to significant increase in the accumulation of ROS levels and apoptotic cell death.
SOD2↓,
ROS↑,
Apoptosis↑,
NOXA↑,
APAF1↑,
BAX↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Bcl-xL↓,
miR-21↓,
Apoptosis↑,
miR-21↓,
TOS↓, while decreasing TOS levels in Jurkat cells
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in-vitro, |
Ovarian, |
MDAH-2774 |
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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/CCND1∅,
CDK6∅,
CDK4∅,
FADD∅,
DR4∅,
DR5∅,
β-catenin/ZEB1↓,
AR↓, Treatment with PLGA-CUR NPs drastically decreases the AR expression level (Figure 5C) compared to free curcumin.
STAT3↓, PLGA-CUR treatment inhibited the expression of STAT3 and phosphorylation of AKT at even the lowest concentration
p‑Akt↓,
Mcl-1↓,
Bcl-xL↓,
cl‑PARP↑, Prostate cancer cells treated with CUR or PLGA-CUR NPs exhibited PARP cleavage and inhibited the expression of anti-apoptotic proteins, Bcl-XL and Mcl-1
miR-21↓, 9-fold reduction in expression of the oncomir, miR-21, in prostate cancer cells (C4-2 and DU-145) t
miR-205↑,
TumCG↓, PLGA-CUR NPs were capable of reducing both in vitro and in vivo prostate cancer cell growth,
TumCP↓, data suggest that curcumin can effectively suppress prostate cancer cell proliferation, invasion, angiogenesis, and metastasis
TumCI↓,
angioG↓,
TumMeta↓,
TumCP↓,
β-catenin/ZEB1↓,
TCF↓, TCF4
miR-21↓,
NKD2↑,
miR-130a↓, main target affecting others
miR-21↓, Curcumin can effectively repress the miR-21/PTEN/Akt molecular pathway to inhibit cell proliferation and induce apoptosis in gastric cancer cells
TumCP↓, Curcumin can inhibit the proliferation, migration, invasion and promote apoptosis of retinoblastoma cells, which function through up-regulating the miR-99a expression and then inhibiting JAK/STAT signaling pathway
TumCMig↓,
TumCI↓,
Apoptosis↑,
miR-99↑,
JAK↓,
STAT↓,
cycD1/CCND1↓, curcumin can suppress the cell proliferation by down-regulations of cyclinD1 and up-regulations of p21 expression.
P21↑,
ChemoSen↑, curcumin combined with chemotherapy drugs may play a better therapeutic effect via JAK/STAT signaling pathway
miR-192-5p↑, curcumin enhanced the expression level of miR−192−5p and decreased the expression of c−Myc.
cMyc↓,
Wnt↓, curcumin suppresses colon cancer by inhibiting Wnt/β-catenin pathway via down-regulating miR-130a
β-catenin/ZEB1↓,
miR-130a↓,
miR-497↑, Curcumin was found to cause the upregulation of miR-497, miR-200c, miR-200b, miR-409-3p, miR‐34, miR‐126, miR-145, miR-206, miR-491, miR-141, miR-429, miR-101, and miR-15a
miR-200c↑,
miR-409-3p↑,
miR-34a↑,
miR-126↑,
miR-145↑,
miR-206↑,
miR-491↑,
miR-141↑,
miR-429↑,
miR-101↑,
miR-15↑,
miR-21↓, and the downregulation of miR-21, miR-155, miR‐221, miR‐222, miR-17-5p, miR-130a, miR-27, and miR-20a.
miR-155↓,
miR-221↓,
miR‐222↓,
miR-17↓,
miR-130a↓,
miR-27a-3p↓,
miR-20↓,
chemoPv↑, Curcumin is well known for its chemopreventive and anti-cancer properties.
AntiCan↑,
*antiOx↑, Mechanistically, curcumin exerts its biological impacts via antioxidant and anti-inflammatory effects through the interaction with various transcription factors and signaling molecules.
*Inflam↓,
miR-21↓, Table 1
miR-34a↑,
miR-200b↑,
miR-27a-3p↓,
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Review, |
Var, |
NA |
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Review, |
AD, |
NA |
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*ROS↓, CUR reduced the production of ROS
*SOD↑, CUR also upregulated the expression of superoxide dismutase (SOD) genes
p16↑, The effects of CUR on gene expression in cancer-associated fibroblasts obtained from breast cancer patients has been examined. CUR increased the expression of the p16INK4A and other tumor suppressor proteins
JAK2↓, CUR decreased the activity of the JAK2/STAT3 pathway
STAT3↓,
CXCL12↓, and many molecules involved in cellular growth and metastasis including: stromal cell-derived factor-1 (SDF-1), IL-6, MMP2, MMP9 and TGF-beta
IL6↓,
MMP2↓,
MMP9↓,
TGF-β↓,
α-SMA↓, These effects reduced the levels of alpha-smooth muscle actin (alpha-SMA) which was attributed to decreased migration and invasion of the cells.
LAMs↓, CUR suppressed Lamin B1 and
DNAdam↑, induced DNA damage-independent senescence in proliferating but not quiescent breast stromal fibroblasts in a p16INK4A-dependent manner.
*memory↑, CUR has recently been shown to suppress memory decline by suppressing beta-site amyloid precursor protein cleaving enzyme 1 (BACE1= Beta-secretase 1, an important gene in AD) expression which is implicated in beta-amyoid pathology in 5xFAD transgenic
*cognitive↑, CUR was found to decrease adiposity and improve cognitive function in a similar fashion as CR in 15-month-old mice.
*Inflam↓, The effects of CUR and CR were positively linked with anti-inflammatory or antioxidant actions
*antiOx↑,
*NO↑, CUR treatment increased nNOS expression, acidity and NO concentration
*MDA↓, CUR treatment resulted in decreased levels of MDA
*ROS↓, CUR treatment was determined to cause reduction of ROS in the AMD-RPEs and protected the cells from H2O2-induced cell death by reduction of ROS levels.
DNMT1↓, CUR has been shown to downregulate the expression of DNA methyl transferase I (DNMT1)
ROS↑, induction of ROS and caspase-3-mediated apoptosis
Casp3↑,
Apoptosis↑,
miR-21↓, CUR was determined to decrease both miR-21 and anti-apoptotic protein expression.
LC3II↓, CUR also induced proteins associated with cell death such as LC3-II and other proteins in U251 cells
ChemoSen↑, The combined CUR and temozolomide treatment resulted in enhanced toxicity in U-87 glioblastoma cells.
NF-kB↓, suppression of NF-kappaB activity
CSCs↓, Dendrosomal curcumin increased the expression of miR-145 and decreased the expression of stemness genes including: NANOG, OCT4A, OCT4B1, and SOX2 [113]
Nanog↓,
OCT4↓,
SOX2↓,
eff↑, A synergistic interaction was observed when emodin and CUR were combined in terms of inhibition of cell growth, survival and invasion.
Sp1/3/4↓, CUR inducing ROS which results in suppression of specificity protein expression (SP1, SP3 and SP4) as well as miR-27a.
miR-27a-3p↓,
ZBTB10↑, downregulation of miR-27a by CUR, increased expression of ZBTB10 occurred
SOX9?, This resulted in decreased SOX9 expression.
ChemoSen↑, CUR used in combination with cisplatin resulted in a synergistic cytotoxic effect, while the effects were additive or sub-additive in combination with doxorubicin
VEGF↓, Some of the effects of CUR treatment are inhibition of NF-κB activity and downstream effector proteins, including: VEGF, MMP-9, XIAP, BCL-2 and Cyclin-D1.
XIAP↓,
Bcl-2↓,
cycD1/CCND1↓,
BioAv↑, Piperine is an alkaloid found in the seeds of black pepper (Piper nigrum) and is known to enhance the bioavailability of several therapeutic agents, including CUR
Hif1a↓, CUR inhibits HIF-1 in certain HCC cell lines and in vivo studies with tumor xenografts. CUR also inhibited EMT by suppressing HIF-1alpha activity in HepG2 cells
EMT↓,
BioAv↓, CUR has a poor solubility in aqueous enviroment, and consequently it has a low bioavailability and therefore low concentrations at the target sites.
PTEN↑, CUR treatment has been shown to result in activation of PTEN, which is a target of miR-21.
VEGF↓, CUR treatment resulted in a decrease of VEGF and activated Akt.
Akt↑,
EZH2↓, CUR also suppressed EZH2 expression by induction of miR-let 7c and miR-101.
NOTCH1↓, The expression of NOTCH1 was inhibited upon EZH2 suppression [
TP53↑, CUR has been shown to activate the TP53/miR-192-5p/miR-215/XIAP pathway in NSCLC.
NQO1↑, CUR can also induce the demethylation of the nuclear factor erythroid-2 (NF-E2) related factor-2 (NRT2) gene which in turn activates (NQO1), heme oxygenase-1 (HO1) and an antioxidant stress pathway which can prevent growth in mouse TRAMP-C1 prostate
HO-1↑,
AR↓,
miR-21↓,
miR-330-5p↑,
TumCG↓,
Apoptosis↑, MP enhanced anti-cancer effects by inducing apoptosis and inhibiting proliferation.
TumCP↓,
ROS↑, MP induced both ROS and NO, upon neutralizing them, there was a partial recovery of apoptosis and proliferation.
NO↑,
Dose↝, MP is a humic matter, shown to contain fulvic acid and humic acid, which are responsible for its biochemical activities.
MMP↓, mitochondrial membrane potential is reduced, cytochrome c is released, the transition pores are opened and calcium is released by the increased NO level which eventually leads to apoptosis
Cyt‑c↑,
SOD↓, SOD activity in Huh-7 cells was found to be decreasing with increasing concentrations of MP
Catalase↓, catalase activity was significantly decreased in all the concentrations of MP that was tested.
GSH↑, Glutathione production was significantly increased with the increasing concentrations of MP. There was a more than 7-fold increase of glutathione production with 100, 500 and 1000 μg/ml of MP
lipid-P↑, lipid peroxidation of the cancer cells was found to be increased in concentration dependent manner.
miR-21↓, MP induces ROS and nitric oxide, enhances the expression of miRNA-22 and decreases the expression of miRNA-21, a known onco-miR.
miR-22↑,
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↓, Inhibitory effects of quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
MAPK↓,
Wnt/(β-catenin)↓, wnt
PSA↓,
VEGF↓,
PARP↑,
Casp3↑,
Casp9↑,
DR5↑,
ROS⇅,
Shh↓,
P53↑, figure 1
P21↑, quercetin regulates p21 expression
EGFR↓,
TumCCA↑, quercetin has cell-specific anti-proliferative impacts via stimulation of cell cycle arrest at the G1 stage.
ROS↑, 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↓,
TumCP↓,
selectivity↑, In breast cancer cells, quercetin inhibits cell proliferation without exerting any cytotoxic impact on normal breast epithelium
PDGF↓, figure 1
EGF↓,
TNF-α↓,
VEGFR2↓,
mTOR↓,
cMyc↓,
MMPs↓,
GRP78/BiP↑,
CHOP↑,
ROS↑, QH decreased the production of reactive oxygen species (ROS) and increased antioxidant capacity in PC3 cells at various concentrations (2.5‑60 µg/ml) with peak inhibition and augmentation changes of 3.22‑ and 3.00‑fold, respectively.
cl‑Casp3↑, activated/cleaved caspase-3 levels were found to be elevated at low concentration of QH (5 and 10 μg/ml) by ~1.5-fold and at higher concentrations (20 and 40 μg/ml) by ~2.7-fold (Fig. 2E). Poly(adenosine diphosphate ribose)
cl‑PARP↑, analysis revealed an increase in PARP cleavage in PC3 cells following QH treatment
miR-21↓, dose-dependent decrease in miR-21 expression, with inhibition rates of 42, 56 and 77% observed at 5, 10 and 20 μg/ml QH, respectively
PDCD4↑,
TAC↑,
tumCV↓, QH inhibits PC3 cell viability.
TumCI↓, QH inhibits the invasive activity of PC3 cells.
AR↓,
PI3K/Akt↓, The combination treatment significantly inhibited both AR and PI3K/Akt pathways compared to control.
miR-21↓,
STAT3↓,
BAD↓,
PRAS40↓,
GSK‐3β↓,
PSA↓,
NKX3.1↑,
Bax:Bcl2↑, a significantly increased ratio of Bax to Bcl-2 protein expression was observed in LAPC-4 cells by the combination treatment compared to Q alone, and a trend to increase in LNCaP cells
miR-19b↓,
miR-148a↓,
AMPKα↓,
TumCP↓, The anti-proliferative activity of arctigenin was 10-20 fold stronger than quercetin in both cell lines.
chemoPv↑, combination of arctigenin and quercetin, that target similar pathways, at low physiological doses, provides a novel regimen with enhanced chemoprevention in prostate cancer.
TumCMig↓, Enhanced inhibition of cell migration
BioAv↓, Resveratrol is poorly bioavailable, and that considered the major hindrance to exert its therapeutic effect, especially for cancer management
BioAv↓, at lower doses (25 mg per healthy subject) demonstrate that the mean proportion of free resveratrol in plasma was 1.7–1.9% with a mean plasma concentration of free resveratrol around 20 nM
Dose↑, Boocock and his colleagues studied the pharmacokinetic of resveratrol; in vitro data showed that minimum of 5 µmol/L resveratrol is essential for the chemopreventive effects to be elicited
eff↑, Despite the low bioavailability of resveratrol, it shows efficacy in vivo. This may be due to the conversion of both glucuronides and sulfate back to resveratrol in target organs such as the liver
eff↑, repeated administration of high doses of resveratrol generates a higher plasma concentration of parent and a much higher concentration of sulfate and glucuronide conjugates in the plasma
Dose↑, The doses tested in this study were 0.5, 1.0, 2.5 or 5.0 g daily for 29 days. No toxicity was detected, but moderate gastrointestinal symptoms were reported for 2.5 and 5.0 g doses
BioAv↑, the co-administration of piperine with resveratrol was used to enhance resveratrol bioavailability
ROS↑, Recent studies have shown that resveratrol increases ROS generation and decreases mitochondrial membrane potential
MMP↓,
P21↑, treatment decreased the viability of melanoma cells by activating the expression of both p21 and p27, which promoted cell cycle arrest.
p27↑,
TumCCA↑,
ChemoSen↑, Additionally, the use of resveratrol with cisplatin in malignant human mesothelioma cells (MSTO-211H and H-2452 cells) synergistically induces cell death by increasing the intracellular ROS level [64].
COX2↓, covers the down-regulation of the products of the following genes, COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA [93].
5LO↓,
VEGF↓,
IL1↓,
IL6↓,
IL8↓,
AR↓,
PSA↓,
MAPK↓, by preventing also the activation of the MAPK and PI3K/Akt signaling pathways, it suppresses HIF-1a and VEGF release in ovarian cancer cells of humans
Hif1a↓,
Glycolysis↓, Resveratrol was found to effectively impede the activation, invasion, migration and glycolysis of PSCs induced by reactive oxygen species (ROS) by down-regulating the expression of microRNA 21 (miR-21)
miR-21↓,
PTEN↑, also by increasing the phosphatise and tensin homolog (PTEN) protein levels
Half-Life↝, 25 mg/70 kg resveratrol administered to healthy human participants, the compound predominantly appeared in the form of glucuronide and sulfate conjugates in serum and urine and reached its peak concentrations in serum about 30 min after ingestion
*IGF-1↓, Brown and colleagues noted how a major decline in circulating insulin-like growth factor (IGF)-I as well as IGF-binding proteins (IGFBP-3) among healthy individuals can be credited to the intake of resveratrol
*IGFBP3↑,
Half-Life↓, Microactive® and Resveratrol SR and manufactured by Bioactives. This compound is capable of sustained release for over 12 h to increase intestinal residence time.
PI3K↓,
Akt↓,
NF-kB↓,
Wnt/(β-catenin)↓,
MAPK↓,
TumCP↓,
TumCCA↑, G0/G1 cell cycle arrest
Apoptosis↑, In T24 and UM-UC-3 human bladder cancer cells, silibinin treatment at a concentration of 10 μM significantly inhibited proliferation, migration, invasion, and induced apoptosis.
p‑EGFR↓,
JAK2↓,
STAT5↓,
cycD1/CCND1↓,
hTERT/TERT↓,
AP-1↓,
MMP9↓,
miR-21↓,
miR-155↓,
Casp9↑,
BID↑,
ERK↓, ERK1/2
Akt2↓,
DNMT1↓,
P53↑,
survivin↓,
Casp3↑,
ROS↑, cytotoxicity of silibinin in Hep-2 cells was associated with the accumulation of intracellular reactive oxygen species (ROS), which could be mitigated by the ROS scavenger NAC.
Showing Research Papers: 1 to 18 of 18
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 18
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Catalase↓, 1, GSH↑, 1, HO-1↑, 1, lipid-P↑, 1, NQO1↑, 1, ROS↑, 9, ROS⇅, 1, SOD↓, 1, SOD2↓, 1, TAC↑, 1, TOS↓, 1,
Mitochondria & Bioenergetics ⓘ
EGF↓, 1, MMP↓, 2, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, cMyc↓, 2, Glycolysis↓, 1, PI3K/Akt↓, 1,
Cell Death ⓘ
Akt↓, 1, Akt↑, 1, p‑Akt↓, 1, APAF1↑, 1, Apoptosis↑, 8, BAD↓, 1, BAX↑, 1, Bax:Bcl2↑, 1, Bcl-2↓, 3, Bcl-xL↓, 2, BID↑, 1, Casp10∅, 1, Casp3↑, 4, cl‑Casp3↑, 1, Casp8∅, 1, Casp9↑, 3, Cyt‑c↑, 2, Diablo↑, 1, DR4∅, 1, DR5↑, 1, DR5∅, 1, FADD∅, 1, hTERT/TERT↓, 1, MAPK↓, 3, Mcl-1↓, 1, miR-497↑, 1, NOXA↑, 1, p27↑, 1, PDCD4↑, 1, Set9↑, 1, survivin↓, 1,
Kinase & Signal Transduction ⓘ
AMPKα↓, 1, SOX9?, 1, Sp1/3/4↓, 2,
Transcription & Epigenetics ⓘ
EZH2↓, 1, miR-145↑, 1, miR-192-5p↑, 1, miR-205↑, 1, miR-21↓, 18, miR-27a-3p↓, 3, miR-409-3p↑, 1, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, GRP78/BiP↑, 1,
Autophagy & Lysosomes ⓘ
LC3II↓, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 2, DNMT1↓, 2, NKX3.1↑, 1, p16↑, 1, P53↑, 2, PARP↑, 1, cl‑PARP↑, 2, TP53↑, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK4∅, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 3, cycD1/CCND1∅, 1, P21↑, 3, TumCCA↑, 4,
Proliferation, Differentiation & Cell State ⓘ
CSCs↓, 1, EMT↓, 2, ERK↓, 1, Gli1↓, 1, GSK‐3β↓, 1, miR-101↑, 1, miR-330-5p↑, 1, miR-34a↑, 2, miR-429↑, 1, miR-99↑, 1, mTOR↓, 2, Nanog↓, 1, NKD2↑, 1, NOTCH1↓, 1, OCT4↓, 1, PI3K↓, 2, PTCH1↓, 1, PTEN↑, 2, Shh↓, 1, SOX2↓, 1, STAT↓, 1, STAT3↓, 3, p‑STAT3↓, 1, STAT5↓, 1, TCF↓, 1, TumCG↓, 2, Wnt↓, 1, Wnt/(β-catenin)↓, 2,
Migration ⓘ
5LO↓, 1, Akt2↓, 1, AP-1↓, 1, CXCL12↓, 1, GLI2↓, 1, LAMs↓, 1, miR-130a↓, 4, miR-141↑, 1, miR-148a↓, 1, miR-155↓, 2, miR-19b↓, 1, miR-20↓, 1, miR-200b↑, 1, miR-200c↑, 1, miR-206↑, 1, miR-22↑, 1, miR-221↓, 1, miR-491↑, 1, miR‐222↓, 1, MMP2↓, 2, MMP9↓, 3, MMPs↓, 1, PDGF↓, 1, TGF-β↓, 1, TumCI↓, 4, TumCMig↓, 3, TumCP↓, 8, TumMeta↓, 1, α-SMA↓, 1, β-catenin/ZEB1↓, 3,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, EGFR↓, 2, p‑EGFR↓, 1, Hif1a↓, 2, miR-126↑, 1, miR-15↑, 1, miR-17↓, 1, NO↑, 1, VEGF↓, 5, VEGFR2↓, 1, ZBTB10↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL1↓, 1, IL6↓, 2, IL8↓, 1, JAK↓, 1, JAK1↓, 1, JAK2↓, 3, NF-kB↓, 3, PSA↓, 3, TNF-α↓, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 4, CDK6∅, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 3, BioAv↑, 2, ChemoSen↑, 4, Dose↑, 2, Dose↝, 1, eff↑, 3, Half-Life↓, 1, Half-Life↝, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
AR↓, 4, EGFR↓, 2, p‑EGFR↓, 1, EZH2↓, 1, hTERT/TERT↓, 1, IL6↓, 2, PSA↓, 3, TP53↑, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, chemoPv↑, 3, PRAS40↓, 1,
Total Targets: 179
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, MDA↓, 1, ROS↓, 2, SOD↑, 1,
Proliferation, Differentiation & Cell State ⓘ
IGF-1↓, 1, IGFBP3↑, 1,
Angiogenesis & Vasculature ⓘ
NO↑, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 2,
Functional Outcomes ⓘ
cognitive↑, 1, memory↑, 1,
Total Targets: 10
Scientific Paper Hit Count for: miR-21, miR-21
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:191 State#:% Dir#:1
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