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⟱

8748-

MeSA,

Methylseleninic acid elevates REDD1 and inhibits prostate cancer cell growth despite AKT activation and mTOR dysregulation in hypoxia

in-vitro,

Pca,

LNCaP

in-vitro,

Pca,

PC3

Hif1a↓, DDIT4?, p‑Akt↑, P70S6K↑, TumCG↓,

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:

Kinase & Signal Transduction(tgid=6) ⓘ

p‑Akt↑, 1, DDIT4?, 1, P70S6K↑, 1,

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

TumCG↓, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,
Total Targets: 5

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