condition found tbRes List
CUR, Curcumin: Click to Expand ⟱
Features:
Curcumin is the main active ingredient in Tumeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.
- Has iron-chelating, iron-chelating properties. Ferritin. But still known to increase Iron in Cancer cells.
- GSH depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises GSH↑ in normal cells.
- Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production
- Inhibition of TrxR, shifting the enzyme from an antioxidant to a prooxidant
- Strong inhibitor of Glo-I, , causes depletion of cellular ATP and GSH
- Curcumin has been found to act as an activator of Nrf2, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown

Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.
• Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.

-Note half-life 6 hrs.
BioAv is poor, use piperine or other enhancers
Pathways:
- induce ROS production at high concentration. Lowers ROS at lower concentrations
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: GSH↓ Catalase↓ HO1↓ GPx↓
but conversely is known as a NRF2↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, uPA↓, VEGF↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK, TrxR**,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


Gli1, glioma-associated oncogene homolog 1: Click to Expand ⟱
Source:
Type: HH
Gli family zinc-finger transcription factors; GLI1‐dependent target genes (CyclinD1, Bcl‐2, Foxm1)

Glioma-associated oncogene homolog 1 (GLI1) is a transcription factor that plays a significant role in the Hedgehog signaling pathway, which is crucial for cell growth, differentiation, and tissue patterning during embryonic development.
GLI1 can promote tumor growth and survival by regulating the expression of genes involved in cell proliferation, apoptosis, and angiogenesis. Its overexpression has been associated with aggressive tumor behavior and poor prognosis in several cancer types.
ts overexpression is often associated with aggressive tumor behavior, poor prognosis, and resistance to therapy
Scientific Papers found: Click to Expand⟱
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↓,
Shh↓,
Gli1↓,
cycD1↓,
Bcl-2↓,
Foxm1↓,
Bax:Bcl2↑,

455- CUR,    Curcumin Affects Gastric Cancer Cell Migration, Invasion and Cytoskeletal Remodeling Through Gli1-β-Catenin
- in-vitro, GC, SGC-7901
Shh↓,
Gli1↓,
Foxm1↓,
β-catenin/ZEB1↓,
TumCMig↓, induced S phase cell cycle arrest
Apoptosis↑,
TumCCA↑,
Wnt↓,
EMT↓,
E-cadherin↑,
Vim↓,

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)↓,
Shh↓,
Smo↓,
Gli1↝,
GLI2↝,

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↓,
Shh↓,
Smo↓,
Gli1↓,
N-cadherin↓,
E-cadherin↑,
Vim↓,

12- CUR,    Curcumin inhibits the Sonic Hedgehog signaling pathway and triggers apoptosis in medulloblastoma cells
- in-vitro, MB, DAOY
HH↓,
Shh↓,
Gli1↓,
PTCH1↓,
cMyc↓,
n-MYC↓,
cycD1↓,
Bcl-2↓,
NF-kB↓,
Akt↓,
β-catenin/ZEB1↓,
survivin↓,

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↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Results for Effect on Cancer/Diseased Cells:
Akt↓,1,   Apoptosis↑,1,   Bax:Bcl2↑,1,   Bcl-2↓,2,   cMyc↓,1,   cycD1↓,2,   E-cadherin↑,2,   EMT↓,2,   Foxm1↓,2,   Gli1↓,5,   Gli1↝,1,   GLI2↝,1,   HH↓,5,   N-cadherin↓,1,   n-MYC↓,1,   NF-kB↓,1,   PTCH1↓,1,   Shh↓,5,   Smo↓,2,   survivin↓,1,   TumCCA↑,1,   TumCMig↓,1,   Vim↓,2,   Wnt↓,1,   Wnt/(β-catenin)↓,1,   β-catenin/ZEB1↓,2,  
Total Targets: 26

Results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: Gli1, glioma-associated oncogene homolog 1
6 Curcumin
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:65  Target#:124  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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