DDIT4 Cancer Research Results

DDIT4, DNA damage-inducible transcript 4; REDD1; RTP801: Click to Expand ⟱
Source:
Type:

DDIT4 (DNA damage-inducible transcript 4; REDD1; RTP801) is a stress-inducible regulatory protein activated by hypoxia, DNA damage, oxidative stress, nutrient deprivation, glucocorticoids and other cellular stresses. DDIT4 generally suppresses mechanistic target of rapamycin complex 1 (mTORC1) signalling, thereby reducing protein synthesis, cell growth and anabolic metabolism while promoting stress adaptation and, in some settings, autophagy. Increased DDIT4 can mediate anticancer effects by inhibiting mTORC1, causing cell-cycle arrest and limiting proliferation; for example, DDIT4 contributes to metformin-induced mTOR inhibition in prostate cancer cells. However, tumour cells may also use DDIT4 to survive hypoxia, metabolic stress or anticancer treatment, and DDIT4 can suppress ER-stress-induced apoptosis in some cancer models. Loss of DDIT4 may alternatively increase mTORC1 activity and proliferation in certain tissues.



Scientific Papers found: Click to Expand⟱
7087- GAR,    Garcinol as an Epigenetic Modulator: Mechanisms of Anti-Cancer Activity and Therapeutic Potential
- Review, Var, NA
HATs↓, Its activities include inhibition of histone acetyltransferases (HATs)
p300↓, By inhibiting HAT enzymes such as p300/CBP and PCAF, garcinol affects the acetylation status of multiple transcription factors and histones,
CBP↓,
NF-kB↓, including NF-κB, STAT3, PI3K/AKT, MAPK, and Wnt/β-catenin, resulting in the suppression of inflammation, angiogenesis, proliferation, and metastasis.
STAT3↓, inhibition of NF-kB, STAT 3, P13/Akt, COX-2, MAPK pathways
PI3K↓,
Akt↓,
MAPK↓,
Wnt↓,
β-catenin/ZEB1↓,
Inflam↓,
angioG↓,
TumCP↓,
TumMeta↓,
TumCCA↑, figure 3
EMT↓, inhibition of epithelial-to-mesenchymal transition (EMT), and cancer stem cell targeting.
CSCs↓,
P53↑, garcinol activates tumor-suppressor proteins such as p53 and inhibits thioredoxin reductase, resulting in elevated intracellular reactive oxygen species (ROS).
TrxR↓,
ROS↑,
JNK↑, The accumulation of ROS subsequently stimulates JNK activation and DNA damage signaling, reinforcing p53 function and promoting apoptosis rather than mere growth inhibition
DNAdam↑,
mt-Apoptosis↑, showing activation of mitochondrial apoptosis through the ROS/JNK/ATF-2/Bcl-2 axis
ER Stress↑, In rhabdomyosarcoma cells, garcinol was also shown to trigger endoplasmic reticulum (ER) stress, elevating the expression of stress-responsive genes such as DDIT3, DDIT4, TRIB3, and SESN2, which facilitate apoptosis under prolonged stress [
CHOP/DDIT3↑,
DDIT4↑,
TRIB3↑,
SESN2↑,
miR-218↑, garcinol upregulates let-c family miRNAs and miR-218 in breast cancer and NSCLC cells by the suppression of EMT and stemness
eff↑, When combined with HDAC inhibitors such as SAHA (Suberoylanilide Hydroxamic Acid), also known by its clinical name Vorinostat, garcinol provides complementary effects on maintaining histone acetylation balance,
ChemoSen↑, when used alongside chemotherapeutic agents such as doxorubicin or cisplatin, garcinol sensitizes resistant tumor cells by restoring apoptotic gene expression and overcoming drug resistance mechanisms
BioAv↓, garcinol suffers from poor aqueous solubility, rapid metabolism, and limited bioavailability,
Half-Life↓,
BioAv↑, These nanoformulations have demonstrated enhanced cellular uptake, prolonged plasma half-life, and superior cytotoxicity in breast, colon, and lung cancer models compared with free garcinol


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

DDIT4↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,   TrxR↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   mt-Apoptosis↑, 1,   CBP↓, 1,   JNK↑, 1,   MAPK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

HATs↓, 1,   miR-218↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

SESN2↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   P53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

CSCs↓, 1,   EMT↓, 1,   p300↓, 1,   PI3K↓, 1,   STAT3↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

TRIB3↑, 1,   TumCP↓, 1,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 1,   eff↑, 1,   Half-Life↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

TRIB3↑, 1,  
Total Targets: 35

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: DDIT4, DNA damage-inducible transcript 4; REDD1; RTP801
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#:1578  State#:%  Dir#:2
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