HH Cancer Research Results

HH, Hedgehog signaling: Click to Expand ⟱
Source: CGL-CF
Type: HH
Sonic hedgehog, Shh; Indian hedgehog, Ihh; Desert hedgehog, Dhh ; Hh signaling pathway is able to regulate the EMT. Hh signaling-related factors, SHH, SMO and GLI1.
Hedgehog signaling is a crucial pathway in embryonic development and tissue homeostasis, but its dysregulation has been implicated in various cancers. The Hedgehog (Hh) pathway is activated by the binding of Hedgehog ligands (such as Sonic Hedgehog, Indian Hedgehog, and Desert Hedgehog) to their receptors, primarily Patched (PTCH) and Smoothened (SMO).

-Hedgehog pathway is crucial for the maintenance of stem cell populations. When deregulated, it can help sustain cancer stem cells (CSCs) that possess self-renewal properties, drive tumor recurrence, and confer resistance to conventional therapies.

-Inhibitors of the pathway, such as vismodegib and sonidegib, have been developed and are used in clinical settings, particularly for treating advanced BCC and other Hedgehog-dependent tumors.
Scientific Papers found: Click to Expand⟱
1- Aco,    Recent development on hyperthermia: An effective cotreatment improving radiotherapy outcome
- in-vitro, PC, PANC1 - in-vitro, Pca, DU145
HH↓, As an adjunct to radiotherapy and chemotherapy, hyperthermia enhances the therapeutic efficacy against both primary and recurrent tumors.
PTCH1↓, The present review explores the mechanisms underlying the synergy between radiotherapy and hyperthermia, while reviewing the outcomes of relevant clinical trials.
Bcl-2↓, Key mechanisms of action include inhibition of DNA repair, reduction of hypoxic tumor cell populations, enhancement of drug uptake and improved perfusion and oxygenation.
Gli1↓,

1353- And,    Andrographolide Induces Apoptosis and Cell Cycle Arrest through Inhibition of Aberrant Hedgehog Signaling Pathway in Colon Cancer Cells
- in-vitro, Colon, HCT116
ChemoSen↑, combination with 5FU, andrographolide exhibited synergistic effect
TumCCA↑, G2/M phase arrest
CDK1↓,
CycB/CCNB1↓,
HH↓, repressed the colon cancer cell growth via inhibiting Hh signaling pathway
Smo↓,
Gli1↓,

5- Api,    Common Botanical Compounds Inhibit the Hedgehog Signaling Pathway in Prostate Cancer
- in-vitro, Pca, NA
HH↓,
Gli1↓,

275- Api,    Apigenin inhibits the self-renewal capacity of human ovarian cancer SKOV3‑derived sphere-forming cells
- in-vitro, Ovarian, SKOV3
HH↓,
CK2↓, CK2α
Gli1↓,

3383- ART/DHA,    Dihydroartemisinin: A Potential Natural Anticancer Drug
- Review, Var, NA
TumCP↓, DHA exerts anticancer effects through various molecular mechanisms, such as inhibiting proliferation, inducing apoptosis, inhibiting tumor metastasis and angiogenesis, promoting immune function, inducing autophagy and endoplasmic reticulum (ER) stres
Apoptosis↑,
TumMeta↓,
angioG↓,
TumAuto↑,
ER Stress↑,
ROS↑, DHA could increase the level of ROS in cells, thereby exerting a cytotoxic effect in cancer cells
Ca+2↑, activation of Ca2+ and p38 was also observed in DHA-induced apoptosis of PC14 lung cancer cells
p38↑,
HSP70/HSPA5↓, down-regulation of heat-shock protein 70 (HSP70) might participate in the apoptosis of PC3 prostate cancer cells induced by DHA
PPARγ↑, DHA inhibited the growth of colon tumor by inducing apoptosis and increasing the expression of peroxisome proliferator-activated receptor γ (PPARγ)
GLUT1↓, DHA was shown to inhibit the activity of glucose transporter-1 (GLUT1) and glycolytic pathway by inhibiting phosphatidyl-inositol-3-kinase (PI3K)/AKT pathway and downregulating the expression of hypoxia inducible factor-1α (HIF-1α)
Glycolysis↓, Inhibited glycolysis
PI3K↓,
Akt↓,
Hif1a↓,
PKM2↓, DHA could inhibit the expression of PKM2 as well as inhibit lactic acid production and glucose uptake, thereby promoting the apoptosis of esophageal cancer cells
lactateProd↓,
GlucoseCon↓,
EMT↓, regulating the EMT-related genes (Slug, ZEB1, ZEB2 and Twist)
Slug↓, Downregulated Slug, ZEB1, ZEB2 and Twist in mRNA level
Zeb1↓,
ZEB2↓,
Twist↓,
Snail?, downregulated the expression of Snail and PI3K/AKT signaling pathway, thereby inhibiting metastasis
CAFs/TAFs↓, DHA suppressed the activation of cancer-associated fibroblasts (CAFs) and mouse cancer-associated fibroblasts (L-929-CAFs) by inhibiting transforming growth factor-β (TGF-β signaling
TGF-β↓,
p‑STAT3↓, blocking the phosphorylation of STAT3 and polarization of M2 macrophages
M2 MC↓,
uPA↓, DHA could inhibit the growth and migration of breast cancer cells by inhibiting the expression of uPA
HH↓, via inhibiting the hedgehog signaling pathway
AXL↓, DHA acted as an Axl inhibitor in prostate cancer, blocking the expression of Axl through the miR-34a/miR-7/JARID2 pathway, thereby inhibiting the proliferation, migration and invasion of prostate cancer cells.
VEGFR2/KDR/Flk1↓, inhibition of VEGFR2-mediated angiogenesis
JNK↑, JNK pathway activated and Beclin 1 expression upregulated.
Beclin-1↑,
GRP78/BiP↑, Glucose regulatory protein 78 (GRP78, an ER stress-related molecule) was upregulated after DHA treatment.
eff↑, results demonstrated that DHA-induced ER stress required iron
eff↑, DHA was used in combination with PDGFRα inhibitors (sunitinib and sorafenib), it could sensitize ovarian cancer cells to PDGFR inhibitors and achieved effective therapeutic efficacy
eff↑, DHA combined with 2DG (a glycolysis inhibitor) synergistically induced apoptosis through both exogenous and endogenous apoptotic pathways
eff↑, histone deacetylase inhibitors (HDACis) enhanced the anti-tumor effect of DHA by inducing apoptosis.
eff↑, DHA enhanced PDT-induced cell growth inhibition and apoptosis, increased the sensitivity of esophageal cancer cells to PDT by inhibiting the NF-κB/HIF-1α/VEGF pathway
eff↑, DHA was added to magnetic nanoparticles (MNP), and the MNP-DHA has shown an effect in the treatment of intractable breast cancer
IL4↓, downregulated IL-4;
DR5↑, Upregulated DR5 in protein, Increased DR5 promoter activity
Cyt‑c↑, Released cytochrome c from the mitochondria to the cytosol
Fas↑, Upregulated fas, FADD, Bax, cleaved-PARP
FADD↑,
cl‑PARP↑,
cycE/CCNE↓, Downregulated Bcl-2, Bcl-xL, procaspase-3, Cyclin E, CDK2 and CDK4
CDK2↓,
CDK4↓,
Mcl-1↓, Downregulated Mcl-1
Ki-67↓, Downregulated Ki-67 and Bcl-2
Bcl-2↓,
CDK6↓, Downregulated of Cyclin E, CDK2, CDK4 and CDK6
VEGF↓, Downregulated VEGF, COX-2 and MMP-9
COX2/PTGS2↓,
MMP9↓,

6- Ba,  Api,  QC,    Common Botanical Compounds Inhibit the Hedgehog Signaling Pathway in Prostate Cancer
- in-vitro, Pca, PC3
HH↓, Common Botanical Compounds Inhibit the Hedgehog Signaling Pathway in Prostate Cancer
Gli1↓, three compounds, apigenin, baicalein, and quercetin, decreased Gli1 mRNA concentration but not Gli reporter activity

7- BBR,    Berberine, a natural compound, suppresses Hedgehog signaling pathway activity and cancer growth
- vitro+vivo, MB, LS174T
HH↓, BBR significantly inhibited the Hh pathway activity.
Gli1∅, observations ruled out the possibility that BBR inhibited the Hh signaling pathway activity by targeting Gli.
PTCH1↓,
Smo↓, BBR inhibited the Hh pathway activity by targeting Smo,
TumCG↓, BBR inhibits the Hh-dependent medulloblastoma cell growth in vitro

8- BetA,    Hedgehog/GLI-mediated transcriptional inhibitors from Zizyphus cambodiana
- in-vitro, PC, HaCaT - in-vitro, Pca, PANC1
HH↓,
Gli1↓, The expressions of GLI-related proteins PTCH and BCL2 were clearly inhibited by 1 or 2.
PTCH1↓,
Bcl-2↓,

17- CBC/D,    CBC-1 as a Cynanbungeigenin C derivative inhibits the growth of colorectal cancer through targeting Hedgehog pathway component GLI 1
- in-vivo, CRC, NA
HH↓, CBC-1 inhibited the proliferation of CRC cells through regulation of mRNA and proteins of the HH pathway
Gli1↓, indicated that CBC-1 regulated this signalling pathway by targeting glioma-associated oncogene (GLI 1
BioAv↓, Cynanbungeigenin C (CBC) is a new type of C21 steroid that has been previously reported for the treatment of medulloblastoma. However, its further investigation was limited by its poor water solubility
TumCP↓, It was found that CBC-1 presented the best inhibitory effect on three types of CRC cell lines, and this effect was superior to that of CBC.

18- CBC/D,    Cynanbungeigenin C and D, a pair of novel epimers from Cynanchum bungei, suppress hedgehog pathway-dependent medulloblastoma by blocking signaling at the level of Gli
- vitro+vivo, MB, NA
HH↓, Mechanistically, CBC and CBD block Hh pathway signaling not through targeting Smo and Sufu, but at the level of Gli
Gli1↓,

6253- CBC/D,    The SHH/GLI signaling pathway: a therapeutic target for medulloblastoma
- Review, MB, NA
Gli1↓, Cynanbungeigenin C (CBC) and D (CBD) have been isolated from Cynanchum bungei Decne plant and have emerged as GLI1 inhibitors although with an unclear mechanism.
Dose↝, Both compounds are able to repress Gli1-luciferase reporter activity (IC50 values of 2.9 and 3.7 μM, respectively), and to inhibit HH signaling in cells expressing D473H and W535L drug-resistant SMO mutants
HH↓,
BBB↑, Of note, pharmacokinetic studies demonstrated the capability of these compounds to cross the BBB

6254- CBC/D,    Cynanchum auriculatum Royle ex Wight., Cynanchum bungei Decne. and Cynanchum wilfordii (Maxim.) Hemsl.: Current Research and Prospects
- Review, Var, NA
*neuroP↑, their dry roots as the bioactive part have been revealed to exhibit anti-tumor, neuroprotection, organ protection, reducing liver lipid and blood lipid, immunomodulatory, anti-inflammatory, and other activities
*Imm↑,
*Inflam↓,
CSCs↓, CA at the dosage of 10 mg/kg was demonstrated to inhibit proliferation and formation of breast cancer stem cells
HH↓, CB at the dosage of 50 mg/kg were revealed to block Hedgehog pathway-dependent medulloblastoma by regulating the level of Gli,
Gli↓,
AST↓, CA at the doses of 4 and 8 g/kg were able to decrease the levels of AST and ALT, improve SOD activity, and reduce malondialdehyde content in the in vivo
ALAT↓,
MDA↓,
hepatoP↑, 500 mg/kg was capable of reducing serum ALT and AST levels in mice with hepatic injury induced by CCl4, revealing its feasibility to exert hepatoprotection effect
*NRF2↑, protect them from oxidative toxicity and inflammatory damages by enhancing Nrf2 and HO-1 expression via the NF-κB signaling pathway
*HO-1↑,
NF-kB?, inhibitory protein of NF-κB
GSK‐3β↓, caudatin of CW during the dose of 12.5–50 μM was uncovered to inhibit GSK3β and β-catenin expression, which was attributed to the suppressive effect on wnt protein target genes COX-2, MMP2, and MMP9
β-catenin/ZEB1↓,
COX2/PTGS2↓,
MMP2↑,
MMP9↓,
BioAv↑, suggesting it could be absorbed and distributed rapidly without long-term accumulation in mice tissue

3861- CUR,    Curcumin as a novel therapeutic candidate for cancer: can this natural compound revolutionize cancer treatment?
- Review, Var, NA
*antiOx↑, fig 1
*Inflam↓,
PI3K↓, By inhibiting pro-survival and pro-inflammatory signaling cascades such as PI3K/Akt/mTOR, MAPK, Wnt/β-catenin, NF-κB, Hedgehog, Notch, and JAK/STAT3, curcumin effectively impedes cancer cell growth and promotes apoptosis.
Akt↓,
mTOR↓,
Wnt↓,
β-catenin/ZEB1↓,
NF-kB↓,
HH↓,
NOTCH↓,
JAK↓,
STAT3↓,
ADAM10↓, Curcumin may inhibit the function of the Notch pathway in cancer by inhibiting Notch pathway activators such as gamma secretases, Notch ligands, or ADAM10.

411- CUR,    Curcumin inhibits the invasion and metastasis of triple negative breast cancer via Hedgehog/Gli1 signaling pathway
- in-vitro, BC, MDA-MB-231
HH↓,
EMT↓,
Gli1↓,

12- CUR,    Curcumin inhibits the Sonic Hedgehog signaling pathway and triggers apoptosis in medulloblastoma cells
- in-vitro, MB, DAOY
HH↓, Curcumin inhibits the Sonic Hedgehog signaling pathway
Shh↓, curcumin inhibited the Shh-Gli1 signaling pathway by downregulating the Shh protein
Gli1↓,
PTCH1↓,
cMyc↓,
n-MYC↓,
cycD1/CCND1↓,
Bcl-2↓,
NF-kB↓,
Akt↓,
β-catenin/ZEB1↓, curcumin reduced the levels of beta-catenin
survivin↓,
Apoptosis↑, Consequently, apoptosis was triggered by curcumin through the mitochondrial pathway via downregulation of Bcl-2, a downstream anti-apoptotic effector of the Shh signaling.
ChemoSen↑, curcumin enhances the killing efficiency of nontoxic doses of cisplatin and gamma-rays.
RadioS↑,
eff↑, we present clear evidence that piperine, an enhancer of curcumin bioavailability in humans

11- CUR,    Curcumin inhibits hypoxia-induced epithelial‑mesenchymal transition in pancreatic cancer cells via suppression of the hedgehog signaling pathway
- in-vitro, PC, PANC1
HH↓, suppression of the hedgehog signaling pathway
Shh↓, Curcumin significantly decreased hypoxia-induced expression levels of SHH, SMO and GLI1.
Smo↓,
Gli1↓,
N-cadherin↓,
E-cadherin↑,
Vim↓,
TumCP↓, inhibit the hypoxia-induced cell proliferation, migration and invasion in pancreatic cancer,
TumCMig↓,
TumCI↓,
EMT↓, mediate the expression of EMT-related factors.
chemoPv↑, Curcumin might be a potential candidate for chemoprevention of this severe disease.

10- CUR,    Curcumin Suppresses Lung Cancer Stem Cells via Inhibiting Wnt/β-catenin and Sonic Hedgehog Pathways
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
HH↓,
Wnt/(β-catenin)↓, curcumin suppressed the activation of both Wnt/β-catenin and Sonic Hedgehog pathways. T
Shh↓,
Smo↓,
Gli1↝,
GLI2↝,
CSCs↓, Curcumin Suppresses Lung Cancer Stem Cells via Inhibiting Wnt/β-catenin and Sonic Hedgehog Pathways
CD133↓, reduced number of CD133-positive cells, decreased expression levels of lung CSC markers,
CSCsMark↓,

9- CUR,    Curcumin Suppresses Malignant Glioma Cells Growth and Induces Apoptosis by Inhibition of SHH/GLI1 Signaling Pathway in Vitro and Vivo
- vitro+vivo, MG, U87MG - vitro+vivo, MG, T98G
HH↓, Both mRNA and protein levels of SHH/GLI1 signaling (Shh, Smo, GLI1) were downregulated in a dose‐ and time‐dependent manner
Shh↓, inhibition of SHH/GLI1 signaling by curcumin may act as a novel mechanism of the apoptosis.
Gli1↓,
cycD1/CCND1↓,
Bcl-2↓,
FOXM1↓,
Bax:Bcl2↑, The Bax/Bcl‐2 ratio (Figure 6D) also gradually increased.
TumCP↓, Curcumin suppressed cell proliferation, colony formation, migration, and induced apoptosis which was mediated partly through the mitochondrial pathway after an increase in the ratio of Bax to Bcl2.
TumCMig↓,
Apoptosis↑,
TumVol↑, Intraperitoneal injection of curcumin in vivo reduced tumor volume,
TumCCA↑, Curcumin Inhibited Proliferation of Human Glioma Cells and induced G2/M Arrest
Casp3↑, level of caspase‐3 increases significantly after curcumin treatment.
OS↑, Curcumin Inhibited GBM Growth in Vivo through SHH/GLI1 Signaling and Prolonged the Survival Period

6235- CUSP9,    Exhaustive in vitro evaluation of the 9-drug cocktail CUSP9 for treatment of glioblastoma
- in-vitro, GBM, NA
tumCV↓,
NF-kB↓, disruption of cell survival pathways, including the NF-kB pathway,
HH↓, Itr-induced Hedgehog pathway inhibition could influence GBM cell proliferation and stem cell-like properties.
5HT↓, Ser, a serotonin uptake inhibitor

6237- CUSP9,    CUSP9* treatment protocol for recurrent glioblastoma: aprepitant, artesunate, auranofin, captopril, celecoxib, disulfiram, itraconazole, ritonavir, sertraline augmenting continuous low dose temozolomide
- NA, GBM, NA
PI3K↓, ARTESUNATE phosphoinositide 3-kinase, Akt, increases ROS, NF-κB activation, TNF-alpha, IL-6, TLR2,
Akt↓,
ROS↑,
NF-kB↓,
TNF-α↓,
TLR2↓,
other↓, APREPITANT 10 hrs NK-1 receptors
TrxR↓, AURANOFIN 10 days thioredoxin, increases ROS, STAT3
STAT3↓,
MMPs↓, CAPTOPRIL 2 hrs ACE, AT1 receptors, MMPs
COX1↓, CELECOXIB 9 hrs COX-1 and -2, carbonic anhydrase -2 and -9
COX2/PTGS2↓,
CA↓,
ALDH↓, DISULFIRAM ALDH, increases ROS
P-gp/ABCB1↓, ITRACONAZOLE P-gp efflux transporters, BCRP, Hedgehog, 5-lipoxygenase
HH↓,
5LO↓,
mTOR↓, RITONAVIR P-gp efflux transporters [weak], Akt, mTOR, cyclin D3, proteasome,
CycD3↓,
Proteasome↓,
other↓, SERTRALINE Akt, mTOR, TCTP
MMP2↓, Captopril inhibited the activity of soluble MMP-2 and MMP-9
MMP9↓,
ALDH↓, Disulfiram potent inhibitor of all isoforms of aldehyde dehydrogenase, ALDH, disulfiram stops ethanol metabolism at the acetaldehyde stage
Copper↓, Since disulfiram chelates Cu++ in the stomach even without adding exogenous Cu

6249- Cyc,    Cyclopamine tartrate, an inhibitor of Hedgehog signaling, strongly interferes with mitochondrial function and suppresses aerobic respiration in lung cancer cells
- in-vitro, NSCLC, A549 - in-vitro, NSCLC, H1299
HH↓, Cyclopamine was the first compound found to inhibit Hh signaling and has been invaluable for understanding the function of Hh signaling in development and cancer.
OCR↓, Our results showed that CycT, like glutamine depletion, caused a substantial decrease in oxygen consumption in a number of NSCLC cell lines,
TumCP↓, suppressed NSCLC cell proliferation, and induced apoptosis.
Apoptosis↑,
ROS↑, we found that CycT increased ROS generation, mitochondrial membrane hyperpolarization, and mitochondrial fragmentation, thereby disrupting mitochondrial function in NSCLC cells.
MMP↑, We found that CycT increases mitochondrial membrane potential substantially in NSCLC cells
mtDam↑,

6243- Cyc,    Inhibition of Hedgehog signaling by direct binding of cyclopamine to Smoothened
- Study, Var, NA
AntiTum↑, The steroidal alkaloid cyclopamine has both teratogenic and antitumor activities arising from its ability to specifically block cellular responses to vertebrate Hedgehog signaling.
HH↓,
Smo↓, In principle, cyclopamine-mediated inhibition of vertebrate Smo activity could perturb any of these cellular events.

6244- Cyc,    Widespread requirement for Hedgehog ligand stimulation in growth of digestive tract tumours
- in-vivo, Var, NA
HH↓, Hh pathway activity, which is suppressible by cyclopamine, a Hh pathway antagonist.
TumCG↓, Cyclopamine also suppresses cell growth in vitro and causes durable regression of xenograft tumours in vivo.

6245- Cyc,    Blockade of Hedgehog Signaling Inhibits Pancreatic Cancer Invasion and Metastases: A New Paradigm for Combination Therapy in Solid Cancers
- vitro+vivo, PC, NA
HH↓, Hh inhibition with cyclopamine resulted in down-regulation of snail and up-regulation of E-cadherin, consistent with inhibition of epithelial-to-mesenchymal transition,
Snail↓,
E-cadherin↑,
EMT↓,
TumCI↓, striking reduction of in vitro invasive capacity
ChemoSen↑, Combination of gemcitabine and cyclopamine completely abrogated metastases while also significantly reducing the size of “primary” tumors.
TumMeta↓, Cyclopamine abrogates metastases in an orthotopic xenograft model of pancreatic cancer and synergizes with gemcitabine
ALDH↓, Cyclopamine treatment preferentially reduces the ALDH-expressing population in pancreatic cancer cells
eff↑, We believe that our results provide a compelling rationale for exploring Hh inhibitors in human pancreatic cancer, particularly from the standpoint of therapy of metastatic disease.

6246- Cyc,    Cyclopamine is a novel Hedgehog signaling inhibitor with significant anti-proliferative, anti-invasive and anti-estrogenic potency in human breast cancer cells
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231
HH↓, cyclopamine, a naturally occurring Hedgehog-specific small-molecule inhibitor, causes profound inhibition of tumor growth.
TumCP↓, cyclopamine displayed a significant potency in suppressing the proliferation of both estrogen-responsive (MCF-7) and estrogen-independent (MDA-MB-231) human breast cancer cells.
TumCCA↓, Cyclopamine induced a robust G1 cell cycle arrest and elicited notable effects on the expression of cyclin D1 through modulation of the MAPK/ERK signaling pathway.
TumCI↓, Cyclopamine also inhibited the invasive ability of both breast cancer cell lines by suppressing the expression levels of NF-κB, MMP2 and MMP9 protein
NF-kB↓,
MMP2↓,
MMP9↓,
ERα/ESR1↓, cyclopamine significantly downregulated the production of estrogen receptor-α protein.
cycD1/CCND1↓, expression level of cyclin D1 decreased in cyclopamine-treated cells.

6248- Cyc,    The Hedgehog Inhibitor Cyclopamine Reduces β-Catenin-Tcf Transcriptional Activity, Induces E-Cadherin Expression, and Reduces Invasion in Colorectal Cancer Cells
- in-vitro, CRC, NA
HH↓, We have previously shown that the Hedgehog (HH) signalling pathway is active in cells from colorectal tumours, and that inhibition of the pathway with cyclopamine induces apoptosis.
Apoptosis↑,
Slug↓, we show that cyclopamine reduces the expression of transcription factors (Slug, Snail and Twist) associated with the epithelial-mesenchymal transition and reduces the invasiveness of colorectal cancer cells in vitro.
Snail↓,
Twist↓,
EMT↓,
β-catenin/ZEB1↓, Cyclopamine Treatment Reduces β-Catenin-Related Transcription in the Colorectal Cancer Cell Line SW480 in a Dose-Dependent Manner
E-cadherin↑, Cyclopamine Treatment Induces the Expression of E-Cadherin in Both Benign and Malignant Colorectal Tumour-Derived Cell Lines and Reduces Invasion in SW480 Cells
TumCI↓,

6250- Cyc,    Dose- and route-dependent teratogenicity, toxicity, and pharmacokinetic profiles of the hedgehog signaling antagonist cyclopamine in the mouse
- in-vivo, Nor, NA
*HH↓, cyclopamine is a potent Hh antagonist and is used experimentally both in vitro and in vivo to investigate the role of Hh signaling in diverse biological processes
*other↑, transient Hh signaling inhibition induces facial clefting anomalies in the mouse that mimic common human birth defects.

6251- Cyc,    I only have eye for ewe: the discovery of cyclopamine and development of Hedgehog pathway-targeting drugs
- Review, Var, NA
HH↓, cyclopamine action remained enigmatic for 30 years, until this steroid alkaloid was found to be the first specific inhibitor of Hedgehog (Hh) signalling

6252- Cyc,    Hedgehog Pathway Inhibitors as Targeted Cancer Therapy and Strategies to Overcome Drug Resistance
- Review, Var, NA
*BioAv↓, poor oral bioavailability, acid sensitivity, and some degrees of specificity of cyclopamine limit its therapeutic usage in clinical study
Smo↓, cyclopamine derivatives targeting SMO to inhibit the Hh signaling
HH↓,
eff↑, Vismodegib (GDC-0449, Erivedge®) has a higher potency and more favorable pharmaceutical properties than cyclopamine.

16- Cyc,  RES,    Resveratrol inhibits the hedgehog signaling pathway and epithelial-mesenchymal transition and suppresses gastric cancer invasion and metastasis
- in-vitro, GC, SGC-7901
HH↓, decrease in Gli-1, Snail and N-cadherin expression, and an increase in E-cadherin expression in the resveratrol and cyclopamine group compared
Gli1↓,
EMT↓, suggesting that resveratrol inhibited the Hh pathway and EMT, as did cyclopamine.
N-cadherin↓,
E-cadherin↑,
Snail↓,
TumCI↓, suppress invasion and metastasis in gastric cancer in vitro.
TumMeta↓, Resveratrol and cyclopamine inhibits the metastasis and invasion of SGC-7901 cells

19- Deg,    Deguelin inhibits proliferation and migration of human pancreatic cancer cells in vitro targeting hedgehog pathway
- in-vitro, PC, Bxpc-3 - in-vitro, PC, PANC1
HH↓, The activation of the hedgehog (Hh) signaling pathway, as well as matrix metalloproteinases (MMP)-2 and MMP-9, was suppressed by deguelin.
Gli1↓,
PTCH1↓,
Sufu↓,
MMP2↓, Deguelin downregulates MMP-2 and MMP-9 in Bxpc-3 and Panc-1 cells
MMP9↓,
PI3K/Akt↓,
HIF-1↓,
VEGF↓,
IKKα↓,
NF-kB↓,
EMT↓,
AMPK↑,
mTOR↓,
survivin↓,
TumCG↓, Deguelin treatment was observed to inhibit growth and induce apoptosis in two PC cell lines (Bxpc-3 and Panc-1)
Apoptosis↑,
TumCMig↓, Deguelin inhibits migration and invasion of PC cells
TumCI↓,

27- EA,    Ellagic acid inhibits human pancreatic cancer growth in Balb c nude mice
- in-vivo, PC, PANC1
HH↓,
Gli1↓, EA caused a significant inhibition in phospho-Akt, Gli1, Gli2, Notch1, Notch3, and Hey1.
GLI2↓,
CDK1/2/5/9↓,
p‑Akt↓,
NOTCH1↓,
Shh↓,
Snail↓,
E-cadherin↑,
NOTCH3↓,
HEY1↓,
TumCG↓, EA resulted in significant inhibition in tumor growth which was associated with suppression of cell proliferation and caspase-3 activation, and induction of PARP cleavage.
TumCP↓,
Casp3↑,
cl‑PARP↑,
Bcl-2↓, EA inhibited the expression of Bcl-2, cyclin D1, CDK2, and CDK6, and induced the expression of Bax in tumor tissues compared to untreated control group
cycD1/CCND1↓,
CDK2↓,
CDK6↓,
BAX↑,
COX2/PTGS2↓, EA inhibited the markers of angiogenesis (COX-2, HIF1α, VEGF, VEGFR, IL-6 and IL-8), and metastasis (MMP-2 and MMP-9) in tumor tissues.
Hif1a↓,
VEGF↓,
VEGFR2/KDR/Flk1↓,
IL6↓,
IL8↓,
MMP2↓,
MMP9↓,
NA↓, EA could effectively inhibit human pancreatic cancer growth by suppressing Akt, Shh and Notch pathways

20- EGCG,    Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer
- in-vivo, Liver, NA - in-vivo, Tong, NA
HH↓,
Gli1↓,
Smo↓,
TNF-α↓,
COX2/PTGS2↓, EGCG inhibits cyclooxygenase-2 without affecting COX-1 expression at both the mRNA and protein levels, in androgen-sensitive LNCaP and androgen-insensitive PC-3
*antiOx↑, EGCG is a well-known antioxidant and it scavenges most free radicals, such as ROS and RNS
Hif1a↓,
NF-kB↓,
VEGF↓,
STAT3↓,
Bcl-2↓,
P53↑, EGCG activates p53 in human prostate cancer cells
Akt↓,
p‑Akt↓,
p‑mTOR↓,
EGFR↓,
AP-1↓,
BAX↑,
ROS↑, apoptosis was convoyed by ROS production and caspase-3 cleavage
Casp3↑,
Apoptosis↑,
NRF2↑, pancreatic cancer cells via inducing cellular reactive oxygen species (ROS) accumulation and activating Nrf2 signaling
*H2O2↓, EGCG plays a role in the inhibition of H2O2 and NO production in human skin [10].
*NO↓, EGCG plays a role in the inhibition of H2O2 and NO production in human skin [10].
*SOD↑, fig 2
*Catalase↑, fig 2
*GPx↑, fig 2
*ROS↓, fig 2

21- EGCG,    Tea polyphenols EGCG and TF restrict tongue and liver carcinogenesis simultaneously induced by N-nitrosodiethylamine in mice
- in-vivo, Liver, NA
HH↓, The up-regulation of self renewal Wnt/β-catenin, Hh/Gli1 pathways and their associated genes Cyclin D1, cMyc and EGFR along with down regulation of E-cadherin seen during the carcinogenesis processes were found to be modulated during the restriction
PTCH1↓,
Smo↓,
Gli1↓,
CD44↓, Both EGCG and TF significantly reduced (P b 0.05) CD44 positive cells in all the treated groups
β-catenin/ZEB1↓, GCG and TF could reduce β-catenin expression and its nu- clear activation in different cancers (

22- EGCG,    Inhibition of sonic hedgehog pathway and pluripotency maintaining factors regulate human pancreatic cancer stem cell characteristics
- in-vitro, PC, CD133+ - in-vitro, PC, CD44+ - in-vitro, PC, CD24+ - in-vitro, PC, ESA+
HH↓, EGCG also inhibited the components of Shh pathway (smoothened, patched, Gli1 and Gli2)
Smo↓,
PTCH1↓,
PTCH2↓,
Gli1↓,
GLI2↓,
Gli↓,
Bcl-2↓, inhibiting the expression of Bcl-2 and XIAP, and activating caspase-3
XIAP↓,
Shh↓,
survivin↓,
Casp3↑,
Casp7↑,
CSCs↓, EGCG inhibited the expression of pluripotency maintaining transcription factors (Nanog, c-Myc and Oct-4), and self-renewal capacity of pancreatic CSCs.
Nanog↓,
cMyc↓,
OCT4↓,
EMT↓, EGCG inhibited EMT by inhibiting the expression of Snail, Slug and ZEB1, and TCF/LEF transcriptional activity,
Snail↓,
Slug↓,
Zeb1↓,
TumCMig↓, significantly reduced CSC’s migration and invasion, suggesting the blockade of signaling involved in early metastasis.
TumCI↓,
eff↑, combination of quercetin with EGCG had synergistic inhibitory effects on self-renewal capacity of CSCs through attenuation of TCF/LEF and Gli activities

23- EGCG,    (-)-Epigallocatechin-3-gallate induces apoptosis and suppresses proliferation by inhibiting the human Indian Hedgehog pathway in human chondrosarcoma cells
- in-vitro, Chon, SW1353 - in-vitro, Chon, CRL-7891
HH↓, EGCG inhibited the human Indian Hedgehog pathway, down-regulated PTCH and Gli-1 levels,
Gli1↓,
PTCH1↓,
Bcl-2↓, Bcl-2 were significantly decreased and the levels of Bax were significantly increased.
BAX↑,
TumCG↓, EGCG is effective for growth inhibition of a chondrosarcoma cell lines in vitro, and suggest that EGCG may be a new therapeutic option for patients with chondrosarcoma.

651- EGCG,    Epigallocatechin-3-Gallate Therapeutic Potential in Cancer: Mechanism of Action and Clinical Implications
ROS↑, mounting evidence that EGCG can stimulate ROS production, which in turn leads to the phosphorylation and activation of AMPK
p‑AMPK↑,
mTOR↓,
FAK↓,
Smo↓,
Gli1↓,
HH↓,
TumCMig↓,
TumCI↓,
NOTCH↓,
JAK↓,
STAT↓,
Bcl-2↓,
Bcl-xL↓,
BAX↑,
Casp9↑,

28- GEN,    Genistein decreases the breast cancer stem-like cell population through Hedgehog pathway
- in-vivo, BC, MCF7
HH↓, own-regulating Hedgehog-Gli1 signaling pathway.
Smo↓,
Gli1↓,
TumCG↓, Genistein inhibited the MCF-7 breast cancer cells’ growth and proliferation and promoted apoptosis.
TumCP↓,
Apoptosis↑,
CSCs↓, genistein inhibits BCSCs by down-regulating Hedgehog-Gli1 signaling pathway.

29- GEN,    Genistein inhibits the stemness properties of prostate cancer cells through targeting Hedgehog-Gli1 pathway
- in-vivo, Pca, 22Rv1 - in-vivo, Pca, DU145
HH↓, Genistein inhibits the stemness properties of prostate cancer cells through targeting Hedgehog-Gli1 pathway
Gli1↓, but also inhibited Hedgehog-Gli1 pathway
CSCs↓, genistein treatment not only led to the down-regulation of PCa CSC markers CD44 in vitro and in vivo
TumCI↓, genistein can inhibit PCa cell invasion by reversing epithelial to mesenchymal transition,
EMT↓,
TumCG↓, genistein treatment inhibited tumor growth of PCa TCs
CD44↓, CD44 was significantly down-regulated after the genistein treatment

166- GEN,  EGCG,  RES,  CUR,    Common botanical compounds inhibit the hedgehog signaling pathway in prostate cancer
- in-vivo, Pca, NA
HH↓, The four compounds, which inhibited Hedgehog signaling in both cell assays (genistein, curcumin, EGCG, and resveratrol), are potentially cheaper and safer alternatives to cyclopamine
Gli1↓, Three compounds, apigenin, baicalein, and quercetin, decreased Gli1 mRNA concentration but not Gli reporter activity.

7299- GlaB,    Functional and therapeutic effects of Glabrescione B delivery by liposomes on Hedgehog-dependent tumors
Gli1↓, Glabrescione B (GlaB), is a small molecule that directly inhibits Gli1/DNA interaction, which showed promising pre-clinical results.
BioAv↓, However, poor solubility limits its clinical translation.
BioAv↑, Lipo/GlaB inhibits Gli1 transcriptional activity more potently than free GlaB and significantly reduces the expression of HH target genes.
HH↓,
BioAv↓, we took advantage of innovative nanopharmaceuticals and we developed a micellar formulation using the biocompatible compound methoxy-poly (ethylene glycol)-cholane (mPEG-Cholane), which increases the GlaB solubility by a 100-fold.

7300- GlaB,  ATO,    Targeting GLI1 and GLI2 with small molecule inhibitors to suppress GLI-dependent transcription and tumor growth
- in-vitro, Var, NA
Gli↓, To date, GANT61, arsenic trioxide (ATO) and Glabrescione B (GlaB) are the only direct GLI antagonists identified.
HH↓, GANT61 and GlaB have been reported to directly bind GLI1 and inhibit the canonical and noncanonical HH pathway
Gli1↓, More recently, the natural isoflavone GlaB was reported as a GLI1 inhibitor that interferes with the GLI1/DNA binding
BioAv↓, Nevertheless, GlaB is characterized by poor aqueous solubility

7301- GlaB,    Gli1/DNA interaction is a druggable target for Hedgehog-dependent tumors
Gli1↓, Remarkably, as a consequence of its robust inhibitory effect on Gli1 activity, Glabrescione B inhibited the growth of Hedgehog-dependent tumor cells in vitro and in vivo
HH↓,

7302- GlaB,    Glabrescione B delivery by self-assembling micelles efficiently inhibits tumor growth in preclinical models of Hedgehog-dependent medulloblastoma
- vitro+vivo, MB, NA
BioAv↑, mPEG5kDa-cholane efficiently enhances the solubility of GlaB, a selective GLI1 inhibitor.
Gli1↓, Glabrescione B (GlaB), a selective GLI1 inhibitor, were investigated in preclinical models of Hh-dependent MB.
TumCG↓, We showed that GlaB reduces tumor growth both in vitro and in vivo in MB and BCC models depending on specific Hh-activating mutation
Dose↝, CD1 WT mice (Charles River Laboratories, Lecco, Italy) treated with mPEG5kDa-cholane/GlaB (9 mg/kg) by i.v. injection.
BBB↑, GlaB loaded in mPEG5kDa-cholane micelles crosses the BBB and inhibits tumor growth in a Hh-dependent MB orthotopic model
HH↓,

31- GlaB,    Gli1/DNA interaction is a druggable target for Hedgehog-dependent tumors
- in-vitro, BCC, NA
HH↓, robust inhibitory effect on Gli1 activity, Glabrescione B inhibited the growth of Hedgehog-dependent tumor cells in vitro and in vivo
Gli1↓, GlaB inhibits Hh signaling by impairing Gli1 function
PTCH1↓,
CSCs↓, as well as the self-renewal ability and clonogenicity of tumor-derived stem cells.

32- GlaB,    Gli1/DNA interaction is a druggable target for Hedgehog-dependent tumors
- in-vivo, MB, NA
HH↓, GlaB inhibits Hh signaling by imparing Gli1/DNA binding and transcriptional activity
Gli1↓, impairing Gli1 activity by interfering with its interaction with DNA
PTCH1↓,
TumCG↓, Glabrescione B inhibited the growth of Hedgehog-dependent tumor cells in vitro and in vivo
CSCs↓, s well as the self-renewal ability and clonogenicity of tumor-derived stem cells.

843- Gra,    Graviola (Annona muricata) Exerts Anti-Proliferative, Anti-Clonogenic and Pro-Apoptotic Effects in Human Non-Melanoma Skin Cancer UW-BCC1 and A431 Cells In Vitro: Involvement of Hedgehog Signaling
- in-vitro, NMSC, A431 - in-vitro, NMSC, UW-BCC1 - in-vitro, Nor, NHEKn
TumCG↓,
TumCCA↑, induce G0/G1 cell cycle arrest
Cyc↓,
Apoptosis↑,
cl‑Casp3↑,
cl‑Casp8↑,
cl‑PARP↑,
HH↓,
Smo↓,
Gli1↓,
GLI2↓,
Shh↓,
Sufu↑,
BAX↑,
Bcl-2↓,
*toxicity↓, normal cells 10-fold higher IC50

30- GSL,    A sesquiterpene lactone from Siegesbeckia glabrescens suppresses Hedgehog/Gli-mediated transcription in pancreatic cancer cells
- in-vitro, PC, PANC1 - in-vitro, PC, AsPC-1
HH↓, suppresses Hedgehog/Gli-mediated transcription in pancreatic cancer cells
Gli1↓,
Shh↓,
cycD1/CCND1↓, which resulted in reduced cancer cell proliferation and downregulated expression of the Gli-target genes, Gli1 and cyclin D1
TumCP↓,

108- GSL,    A sesquiterpene lactone from Siegesbeckia glabrescens suppresses Hedgehog/Gli-mediated transcription in pancreatic cancer cells
- in-vitro, PC, PANC1 - in-vitro, PC, AsPC-1 - in-vitro, PC, C3H10T1/2
HH↓, GSL suppressed Gli-mediated transcriptional activity in human pancreatic cancer PANC-1 and AsPC-1 cells, which resulted in reduced cancer cell proliferation and downregulated expression of the Gli-target genes, Gli1 and cyclin D1.
Gli1↓,
cycD1/CCND1↓,
TumCP↓, GSL dose-dependently suppressed proliferation of the pancreatic cancer cells, with 50% inhibitory concentration (IC50) values of 6.9 and 5.1 µM in PANC-1 and AsPC-1

7468- HNK,    Honokiol and Its Emerging Role in Breast Cancer Therapy
- Review, BC, NA
*ROS↓, HNK inhibits essential oncogenic pathways and reduces oxidative stress, inflammation, metabolic reprogramming, and cancer stemness.
*Inflam↓,
CSCs↓,
ChemoSen↑, HNK demonstrates synergistic activity with chemotherapy, endocrine therapy, targeted therapy, and immune checkpoint inhibitors, increasing sensitivity to treatment across models of ER+, PR+, and HER2+ BrCas, as well as triple-negative breast cancers
BioAv↑, Nanotechnological delivery systems enhance the solubility, bioavailability, and intratumoral accumulation of HNK, increasing its translational capacity.
ROS↑, HNK increases intracellular reactive oxygen species (ROS) levels in cancer cells, coinciding with a time-dependent loss of mitochondrial membrane potential (ΔΨm), indicating that ROS production is closely linked to mitochondrial damage
MMP↓,
mtDam↑,
TumCCA↑, HNK causes G0/G1 cell cycle arrest by downregulating cyclin D1 and CDK4, as well as promoting intrinsic apoptosis-like pathways marked by increases in caspase-3 and caspase-9 activities
cycD1/CCND1↓,
CDK4↓,
Casp3↑,
Casp9↑,
Bcl-2↓, reducing the anti-apoptotic Bcl-2 and Bcl-xL, and increasing the pro-apoptotic Bax
Bcl-xL↓,
BAX↑,
p‑STAT3↓, HNK suppresses the phosphorylation of STAT3 in MDA-MB-231
AMPK↑, HNK was found to activate the LKB1–AMPK axis and induce miR-34a expression in MCF7, SKBR3, and SUM149 cells, thereby inhibiting EMT, stemness, and oncogenic leptin signaling in an LKB1-dependent manner
miR-34a↑,
EMT↓,
HH↓, HNK can induce apoptosis by suppressing essential components of the Hh pathway, including SHH [28], Gli1, and Ptch1 [26], as well as downregulating NF-κB
Shh↓,
Gli1↓,
PTCH1↓,
NF-kB↓,
TNF-α↓, reduces the production of inflammatory cytokines, including TNF-α and IL-6
IL6↓,
Glycolysis↓, HNK suppresses HIF-1α-controlled glycolysis by downregulating glycolytic metabolic enzymes, disrupting glucose uptake, and inhibiting tumor growth.
GlucoseCon↓,
BioAv↓, This limitation is primarily attributed to pharmacokinetic challenges, including poor aqueous solubility, low oral bioavailability, rapid metabolism, and the lack of standardized dosing regimens,
BioAv↓, Preclinical studies demonstrate that following oral administration at 40 mg/kg, HNK is rapidly absorbed (Tmax ≈ 20 min) but exhibits low systemic exposure [75], due to extensive first-pass metabolism and high hepatic extraction
Half-Life↝, While the plasma elimination half-life is moderately prolonged (t½ ≈ 290 min),


Showing Research Papers: 1 to 50 of 71
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 71

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

NA↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Copper↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↑, 6,   TrxR↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,   MMP↑, 1,   mtDam↑, 2,   OCR↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   AMPK↑, 2,   p‑AMPK↑, 1,   cMyc↓, 2,   GlucoseCon↓, 2,   Glycolysis↓, 2,   lactateProd↓, 1,   PI3K/Akt↓, 1,   PKM2↓, 1,   PPARγ↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 5,   p‑Akt↓, 2,   Apoptosis↑, 9,   BAX↑, 6,   Bax:Bcl2↑, 1,   Bcl-2↓, 12,   Bcl-xL↓, 2,   Casp3↑, 5,   cl‑Casp3↑, 1,   Casp7↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 2,   CK2↓, 1,   Cyt‑c↑, 1,   DR5↑, 1,   FADD↑, 1,   Fas↑, 1,   HEY1↓, 1,   JNK↑, 1,   Mcl-1↓, 1,   p38↑, 1,   Proteasome↓, 1,   survivin↓, 3,  

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 2,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,   GRP78/BiP↑, 1,   HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   cl‑PARP↑, 3,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CDK1/2/5/9↓, 1,   CDK2↓, 2,   CDK4↓, 2,   Cyc↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 7,   CycD3↓, 1,   cycE/CCNE↓, 1,   TumCCA↓, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ALDH↓, 3,   CD133↓, 1,   CD44↓, 2,   CSCs↓, 8,   CSCsMark↓, 1,   EMT↓, 10,   FOXM1↓, 1,   Gli↓, 3,   Gli1↓, 34,   Gli1↝, 1,   Gli1∅, 1,   GSK‐3β↓, 1,   HH↓, 49,   miR-34a↑, 1,   mTOR↓, 4,   p‑mTOR↓, 1,   n-MYC↓, 1,   Nanog↓, 1,   NOTCH↓, 2,   NOTCH1↓, 1,   NOTCH3↓, 1,   OCT4↓, 1,   PI3K↓, 3,   PTCH1↓, 11,   PTCH2↓, 1,   Shh↓, 9,   Smo↓, 12,   STAT↓, 1,   STAT3↓, 3,   p‑STAT3↓, 2,   Sufu↓, 1,   Sufu↑, 1,   TumCG↓, 10,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,   AP-1↓, 1,   AXL↓, 1,   CA↓, 1,   Ca+2↑, 1,   CAFs/TAFs↓, 1,   E-cadherin↑, 5,   FAK↓, 1,   GLI2↓, 3,   GLI2↝, 1,   Ki-67↓, 1,   MMP2↓, 4,   MMP2↑, 1,   MMP9↓, 6,   MMPs↓, 1,   N-cadherin↓, 2,   Slug↓, 3,   Snail?, 1,   Snail↓, 5,   TGF-β↓, 1,   TumCI↓, 9,   TumCMig↓, 5,   TumCP↓, 10,   TumMeta↓, 3,   Twist↓, 2,   uPA↓, 1,   Vim↓, 1,   Zeb1↓, 2,   ZEB2↓, 1,   β-catenin/ZEB1↓, 5,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   EGFR↓, 1,   HIF-1↓, 1,   Hif1a↓, 3,   VEGF↓, 4,   VEGFR2/KDR/Flk1↓, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,   GLUT1↓, 1,   P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2/PTGS2↓, 5,   IKKα↓, 1,   IL4↓, 1,   IL6↓, 2,   IL8↓, 1,   JAK↓, 2,   M2 MC↓, 1,   NF-kB?, 1,   NF-kB↓, 8,   TLR2↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1,   ADAM10↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 2,   ERα/ESR1↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 6,   BioAv↑, 4,   ChemoSen↑, 4,   Dose↝, 2,   eff↑, 10,   Half-Life↝, 1,   RadioS↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   EGFR↓, 1,   ERα/ESR1↓, 1,   FOXM1↓, 1,   IL6↓, 2,   Ki-67↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,   chemoPv↑, 1,   hepatoP↑, 1,   OS↑, 1,   TumVol↑, 1,  
Total Targets: 173

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 1,   GPx↑, 1,   H2O2↓, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 2,   SOD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

HH↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,   Inflam↓, 3,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,   toxicity↓, 1,  
Total Targets: 16

Scientific Paper Hit Count for: HH, Hedgehog signaling
10 Cyclopamine
8 Curcumin
6 Resveratrol
6 EGCG (Epigallocatechin Gallate)
6 Glabrescione B
4 Cynanbungeigenin C (CBC) and D (CBD)
3 Apigenin (mainly Parsley)
3 Genistein (soy isoflavone)
3 itraconazole
3 Sulforaphane (mainly Broccoli)
2 Quercetin
2 CUSP9
2 Rosmarinic acid
1 Acoschimperoside P, 2’-acetate
1 Andrographis
1 Artemisinin
1 Baicalein
1 Berberine
1 Betulinic acid
1 Deguelin
1 Ellagic acid
1 Arsenic trioxide
1 Graviola
1 Germacranolide sesquiterpene lactone
1 Siegesbeckia glabrescens
1 Honokiol
1 Inoscavin A
1 isoorientin
1 Physalin F & B
1 Silymarin (Milk Thistle) silibinin
1 Saikosaponin B1 and D
1 Sutherlandioside D
1 Thymoquinone
1 Vitamin D3
1 Vitexin
1 Isovitexin
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#:141  State#:%  Dir#:1
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