GLI2 Cancer Research Results
GLI2, GLI2: Click to Expand ⟱
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GLI1, GLI2, and GLI3 are key downstream effectors of the Hh signaling pathway, acting as nuclear transcription factors that bind to promoters to regulate target gene expression. Highly expressed genes in human gliomas.
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Scientific Papers found: Click to Expand⟱
ROS↑, Baicalein initially incited the formation of ROS, which subsequently aimed at endoplasmic reticulum stress and stimulated the Ca2+/-reliant mitochondrial death pathway.
ER Stress↑,
Ca+2↑,
MMPs↓,
Cyt‑c↑, cytochrome C release
Casp3↑,
ROS↑, Baicalein on apoptosis in human bladder cancer 5637 cells was investigated, and it was found that it induces ROS generation
DR5↑, Baicalein activates DR5 up-regulation
ROS↑, MCF-7 cells by inducing mitochondrial apoptotic cell death. It does this by producing ROS, such as hydroxyl radicals, and reducing Cu (II) to Cu (I) in the Baicalein–Cu (II) system
BAX↑,
Bcl-2↓,
MMP↓,
Casp3↑,
Casp9↑,
P53↑,
p16↑,
P21↑,
p27↑,
HDAC10↑, modulating the up-regulation of miR-3178 and Histone deacetylase 10 (HDAC10), which accelerates apoptotic cell death
MDM2↓, MDM2-mediated breakdown
Apoptosis↑,
PI3K↓, baicalein-influenced apoptosis is controlled via suppression of the PI3K/AKT axis
Akt↓,
p‑Akt↓, by reducing the concentrations of p-Akt, p-mTOR, NF-κB, and p-IκB while increasing IκB expression
p‑mTOR↓,
NF-kB↓,
p‑IκB↓,
IκB↑,
BAX↑,
Bcl-2↓,
ROS⇅, Based on its metabolic activities and intensity, Baicalein can act as an antioxidant and pro-oxidant.
BNIP3↑, Baicalein also increases the production of BNIP3 which is a protein stimulated by ROS and promotes apoptosis
p38↑,
12LOX↓, inhibition of 12-LOX (Platelet-type 12-Lipoxygenase)
Mcl-1↓,
Wnt?, decreasing Wnt activity
GLI2↓, Baicalein significantly reduced the presence of Gli-2, a crucial transcription factor in the SHH pathway
AR↓, downregulating the androgen receptor (AR)
eff↑, PTX/BAI NE could increase intracellular ROS levels, reduce cellular glutathione (GSH) levels, and trigger caspase-3 dynamism in MCF-7/Tax cells. Moreover, it exhibited higher efficacy in inhibiting tumors in vivo
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↑,
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↓, 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↓,
IL6↓,
IL8↓,
MMP2↓,
MMP9↓,
NA↓, EA could effectively inhibit human pancreatic cancer growth by suppressing Akt, Shh and Notch pathways
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in-vitro, |
PC, |
CD133+ |
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in-vitro, |
PC, |
CD44+ |
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in-vitro, |
PC, |
CD24+ |
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in-vitro, |
PC, |
ESA+ |
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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
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in-vitro, |
NMSC, |
A431 |
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in-vitro, |
NMSC, |
UW-BCC1 |
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in-vitro, |
Nor, |
NHEKn |
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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
HH↓, 1, 9, 17, and 18 decreased Hh-related component expressions.
Gli1↓,
GLI2↓, We identified zerumbone (1), zerumbone epoxide (2), staurosporinone (9), 6-hydroxystaurosporinone (10), arcyriaflavin C (11) and 5,6-dihydroxyarcyriaflavin A (12) as inhibitors of GLI-mediated transcription.
PTCH1↓,
Bcl-2↓,
*antiOx↑, Resveratrol is a natural compound with notable health benefits, such as anti-inflammatory, antioxidant, and chemopreventive properties.
*Inflam↓,
*chemoPv↑,
CSCs↓, It has shown potential in inhibiting tumorigenesis and tumour progression via targeted therapy, specifically by targeting cancer stem cells (CSCs)
Wnt↓, Three papers reported on the effects on resveratrol on Wnt/ β-catenin pathway
β-catenin/ZEB1↓,
NOTCH↓, 3 papers on Notch pathway
PI3K↓, 3 papers on PI3K/Akt/mTOR pathway
Akt↓,
mTOR↓,
GSK‐3β↝, Akt/GSK β/snail pathway
Snail↓,
HH↓, 4 papers on Hedgehog pathway
p‑GSK‐3β↓, It downregulated p-AKT, p-GSK3β, Snail and N-cadherin in a dose-dependent manner, indicating its role in modulating the Akt/GSK3β/snail signalling pathway to reverse EMT
N-cadherin↓,
EMT↓,
CD133↓, This further reduced CSC markers CD133, CD44, ALDH1A1, OCT4, SOX2 and β-catenin
CD44↓,
ALDH1A1↓,
OCT4↓,
SOX4↓,
Shh↓, Sun et al., reported that resveratrol downregulated SHH, SMO, Gli1 and Gli2 proteins on renal CSC, reducing the number and size of renal cancer cell spheres and decreasing expression of stemness markers CD44 and CD133
Smo↓,
Gli1↓,
GLI2↓,
CSCs↓, Salinomycin, a monocarboxylic polyether antibiotic isolated from Streptomyces albus, can precisely kill cancer stem cells (CSCs), particularly BCSCs, by various mechanisms, including apoptosis, autophagy, and necrosis.
Apoptosis↑,
TumAuto↑,
necrosis↑,
TumCP↓, salinomycin can inhibit cell proliferation, invasion, and migration in BC and reverse the immune-inhibitory microenvironment to prevent tumor growth and metastasis.
TumCI↓,
TumCMig↓,
TumCG↓,
TumMeta↓,
eff↑, Salinomycin is over 100 times more effective against BCSCs than paclitaxel, the traditional chemotherapy drug for the treatment of BC
Bcl-2↓, downregulation of Bcl-2 expression, and decreases their migration capacity, which is accompanied by downregulation of c-Myc and Snail expression
cMyc↓,
Snail↓,
ALDH↓, salinomycin reduces aldehyde dehydrogenase activity and the expression of MYC, AR, and ERG; it induces oxidative stress and inhibits nuclear factor (NF)-κB activity
Myc↓,
AR↓,
ROS↑, Salinomycin also induces autophagy by increasing intracellular ROS level, which is accompanied by MAPK signaling pathway activation
NF-kB↓,
PTCH1↓, significantly reduces tumor growth, which is accompanied by decreased PTCH, SMO, Gli1, and Gli2 expression
Smo↓,
Gli1↓,
GLI2↓,
Wnt↓, Figure 2
mTOR↓,
GSK‐3β↓,
cycD1/CCND1↓,
survivin↓,
P21↑,
p27↑,
CHOP↑,
Ca+2↑, cytosolic
DNAdam↑,
Hif1a↓,
VEGF↓,
angioG↓,
MMP↓, salinomycin can affect the cell membrane potential and reduce the level of ATP to induce mitophagy and mitoptosis.
ATP↓,
p‑P53↑, Salinomycin increases DNA breaks in BC cells as well as the expression of phosphorylated p53 and γH2AX in Hs578T cells.
γH2AX↑,
ChemoSen↑, Table 3 Synergistic anticancer co-action of salinomycin with other agents in BC.
HH↓, Hedgehog pathway blockade by SFN at a dose of 20 mg/kg resulted in a 45 % reduction in growth of pancreatic cancer tumors and reduced expression of Shh pathway components, Smo, Gli 1, and Gli 2 in mouse tissues.
Smo↓,
Gli1↓,
GLI2↓,
Shh↓,
VEGF↓, SFN inhibited the expression of pluripotency maintaining transcription factors Nanog and Oct-4 and angiogenic markers VEGF and PDGFRα which are downstream targets of Gli transcription
PDGFRA↓,
EMT↓, SFN treatment resulted in a significant reduction in EMT markers Zeb-1, which correlated with increase in E-Cadherin expression suggesting the blockade of signaling involved in early metastasis.
Zeb1↓,
Bcl-2↓, SFN downregulated the expression of Bcl-2 and XIAP to induce apoptosis.
XIAP↓,
E-cadherin↑,
OCT4↓,
Nanog↓,
TumCG↑, SFN results in marked reduction in EMT, metastatic, angiogenic markers with significant inhibition in tumor growth in mice.
CSCs↓, A number of studies have indicated that sulforaphane may target CSCs
ChemoSen↑, Combination therapy with sulforaphane and chemotherapy in preclinical settings has shown promising results.
NF-kB↓, downregulation of NF-kB activity by sulforaphane
Shh↓, Inhibits SHH pathway (Smo, Gli1, Gli2)
Smo↓,
Gli1↓,
GLI2↓,
PI3K↓, Inhibits PI3K/AKT pathway
Wnt↓, Inhibits Wnt/b-catenin pathway
β-catenin/ZEB1↓,
Nanog↓, sulforaphane was found to reduce the expression of SHH pathway components, as well as downstream target genes (e.g.,Nanog, Oct-4, VEGF and ZEB-1)
COX2↓, han
et al. suggested that sulforaphane inhibited the
EMT process via the COX-2/MMP2,9/ZEB1,
Snail and miR-200c/ZEB1 pathways,
Zeb1↓,
Snail↓,
ChemoSideEff↓, More importantly, the combination therapy abolished tumor-initiating potential in vivo, without inducing additional side effects
eff↑, Broccoli sprouts contain approximately 20-times more glucoraphanin than broccoli, which represents typically 74% of all glucosinolates in the sprouts
*BioAv↑, Again, the bioavailability of sulforaphane from broccoli sprouts or broccoli sprout preparations heavily relies on the presence of plant myrosinase.
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in-vitro, |
PC, |
PanCSC |
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in-vitro, |
Nor, |
HPNE |
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in-vitro, |
Nor, |
HNPSC |
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CSCs↓, In an in vitro model, human pancreatic CSCs derived spheres were significantly inhibited on treatment with SFN
Shh↓, SFN inhibited the components of Shh pathway and Gli transcriptional activity
Gli↓,
Nanog↓, suppressing the expression of pluripotency maintaining factors (Nanog and Oct-4) as well as PDGFRα and Cyclin D1
OCT4↓,
PDGFRA↓,
cycD1/CCND1↑,
Apoptosis↑, SFN induced apoptosis by inhibition of BCL-2 and activation of caspases
Casp↑,
Smo↓, SFN inhibited the expression of Smo, Gli1 and Gli2.
Gli1↓,
GLI2↓,
Bcl-2↓, SFN induced apoptosis in pancreatic CSCs by inhibiting Bcl-2 expression and through the activation of caspase 3/7
Casp3↑,
Casp7↑,
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vitro+vivo, |
RCC, |
769-P |
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in-vitro, |
RCC, |
786-O |
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in-vitro, |
RCC, |
ACHN |
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in-vitro, |
RCC, |
OS-RC-2 |
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HH↓,
Gli1↓, downregulation of GLI1 and BCL2,
GLI2↓, silibinin induces apoptosis of RCC cells through inhibition of the mTOR-GLI1‑BCL2 pathway.
mTOR↓,
Bcl-2↓,
Apoptosis↑, Silibinin induces the apoptosis of RCC cells involving activation of caspase-3 and PARP
Casp3↑,
PARP↑,
TumCG↓, Silibinin inhibits the growth of RCC xenografts in vivo
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in-vivo, |
RCC, |
NA |
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in-vivo, |
BCC, |
NA |
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HH↓,
GLI2↓,
Shh↓,
Gli1↓, topical vitamin D3 treatment of existing murine BCC tumors significantly decreases Gli1 and Ki67 staining.
Ki-67↓,
TumCP↓, Vitamin D3 inhibits proliferation of BCC cell lines
Showing Research Papers: 1 to 13 of 13
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned ⓘ
NA↓, 1,
Redox & Oxidative Stress ⓘ
ROS↑, 5, ROS⇅, 1, SOD2↓, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, MMP↓, 2, XIAP↓, 2,
Core Metabolism/Glycolysis ⓘ
12LOX↓, 1, AMPK↑, 1, cMyc↓, 2,
Cell Death ⓘ
Akt↓, 2, p‑Akt↓, 2, Apoptosis↑, 6, BAX↑, 4, Bcl-2↓, 10, Casp↑, 1, Casp3↑, 6, cl‑Casp3↑, 1, Casp7↑, 2, cl‑Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 2, Diablo↑, 1, DR5↑, 1, HEY1↓, 1, Mcl-1↓, 1, MDM2↓, 1, Myc↓, 1, necrosis↑, 1, p27↑, 2, p38↑, 1, survivin↓, 2,
Kinase & Signal Transduction ⓘ
Sp1/3/4↓, 1,
Transcription & Epigenetics ⓘ
miR-21↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 1,
Autophagy & Lysosomes ⓘ
BNIP3↑, 1, TumAuto↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 2, p16↑, 1, P53↑, 1, p‑P53↑, 1, PARP↑, 1, cl‑PARP↑, 2, γH2AX↑, 1,
Cell Cycle & Senescence ⓘ
CDK1/2/5/9↓, 1, CDK2↓, 1, Cyc↓, 1, cycD1/CCND1↓, 2, cycD1/CCND1↑, 1, P21↑, 2, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ALDH↓, 1, ALDH1A1↓, 1, CD133↓, 1, CD44↓, 1, CSCs↓, 5, EMT↓, 3, Gli↓, 2, Gli1↓, 12, GSK‐3β↓, 1, GSK‐3β↝, 1, p‑GSK‐3β↓, 1, HDAC10↑, 1, HH↓, 8, mTOR↓, 4, p‑mTOR↓, 1, Nanog↓, 4, NOTCH↓, 1, NOTCH1↓, 1, NOTCH3↓, 1, OCT4↓, 4, PDGFRA↓, 2, PI3K↓, 3, PTCH1↓, 4, PTCH2↓, 1, Shh↓, 8, Smo↓, 7, p‑STAT3↓, 1, Sufu↑, 1, TumCG↓, 4, TumCG↑, 1, Wnt?, 1, Wnt↓, 3,
Migration ⓘ
Ca+2↑, 2, E-cadherin↑, 2, GLI2↓, 13, Ki-67↓, 1, MMP2↓, 2, MMP9↓, 2, MMPs↓, 1, N-cadherin↓, 1, Slug↓, 1, Snail↓, 5, SOX4↓, 1, TumCI↓, 2, TumCMig↓, 2, TumCP↓, 3, TumMeta↓, 1, Zeb1↓, 3, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, EGFR↓, 1, Hif1a↓, 2, VEGF↓, 4, VEGFR2↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, IL6↓, 1, IL8↓, 1, IκB↑, 1, p‑IκB↓, 1, JAK1↓, 1, JAK2↓, 1, NF-kB↓, 3,
Hormonal & Nuclear Receptors ⓘ
AR↓, 2, CDK6↓, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 2, eff↑, 4,
Clinical Biomarkers ⓘ
AR↓, 2, EGFR↓, 1, IL6↓, 1, Ki-67↓, 1, Myc↓, 1,
Functional Outcomes ⓘ
chemoPv↑, 1, ChemoSideEff↓, 1,
Total Targets: 125
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1,
Functional Outcomes ⓘ
chemoPv↑, 1, toxicity↓, 1,
Total Targets: 5
Scientific Paper Hit Count for: GLI2, GLI2
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#:353 State#:% Dir#:1
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