IRF1 Cancer Research Results

IRF1, interferon regulatory factor 1: Click to Expand ⟱
Source:
Type:

IRF1 (interferon regulatory factor 1) is a transcription factor induced by interferons, pattern-recognition signalling, inflammatory cytokines and DNA damage. IRF1 activates genes involved in innate and adaptive immunity, antigen processing and presentation, growth arrest and programmed cell death. In many cancers, IRF1 expression or function is reduced, deleted or inhibited, which can weaken tumour immune surveillance and permit proliferation, survival and treatment resistance. Restoration or activation of IRF1 can increase MHC class I antigen presentation, support cytotoxic immune responses, induce cell-cycle arrest and promote apoptosis or other inflammatory forms of tumour-cell death. The typical cancer-associated direction is therefore commonly down or functionally suppressed, while the desired anticancer modulation is generally up or restoration of IRF1 activity. However, because IRF1 also regulates inflammatory and immune-checkpoint genes, its effects can vary with tumour type and immune context.



Scientific Papers found: Click to Expand⟱
7137- GI,    6-Shogaol from dried ginger inhibits growth of prostate cancer cells both in vitro and in vivo through inhibition of STAT3 and NF-κB signaling
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - vitro+vivo, Pca, HMVP2
STAT3↓, Mechanistic studies revealed that 6-SHO reduced constitutive and interleukin (IL)-6-induced STAT3 activation and inhibited both constitutive and TNF-α-induced NF-κB activity in these cells.
TNF-α↓,
NF-kB↓,
cycD1/CCND1↓, 6-SHO decreased the level of several STAT3 and NF-κB-regulated target genes at the protein level, including cyclin D1, survivin, and cMyc
survivin↓,
cMyc↓,
IL7↓, modulated mRNA levels of chemokine, cytokine, cell cycle, and apoptosis regulatory genes (IL-7, CCL5, BAX, BCL2, p21, and p27)
RANTES↓, 6-SHO decreased the mRNA expression of IL-7 and CCL5 in both DU145 and LNCaP cells.
BAX↑,
Bcl-2↓,
P21↑, 6-SHO increased the expression of p21, p27, SOCS1 and IRF1
p27/CDKN1B↑,
SOCS1↑,
IRF1↑,
eff↑, these results demonstrate that 6-GIN and 6-PAR have the ability to block growth and reduce survival of both human and mouse PCa cells but that they are both less potent than 6-SHO
TumVol↓, treatment with 6-SHO produced statistically significant decreases in tumor volume at both the 50 and 100 mg/kg doses (62% and 73%, respectively; p<0.05)
TumW↓, tumor weights were also reduced at both doses of 6-SHO (48% and 65% reduction, respectively)
toxicity↓, Taken together, these data demonstrate that 6-SHO has potent in vivo antitumor activity at the doses tested and is free of apparent adverse effects.


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) ⓘ

IL7↓, 1,   IRF1↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,  

Cell Death(tgid=5) ⓘ

BAX↑, 1,   Bcl-2↓, 1,   p27/CDKN1B↑, 1,   survivin↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,  

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

STAT3↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NF-kB↓, 1,   RANTES↓, 1,   SOCS1↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,  

Functional Outcomes(tgid=23) ⓘ

toxicity↓, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: IRF1, interferon regulatory factor 1
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#:1585  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page