6IL Cancer Research Results

6IL, 6-Iodolactone: Click to Expand ⟱
Source:
Type:

6-Iodolactone - 6-Iodo-5-Hydroxy-8,11,14-Eicosatrienoic Acid δ-Lactone

Alternative Names: 6-Iodolactone, 6IL, 6-iodo-5-hydroxy-8,11,14-eicosatrienoic acid δ-lactone

Type: Iodolipid / iodinated arachidonic-acid derivative / bioactive lipid metabolite

Formation: 6-IL is formed by iodination of arachidonic acid and has been detected in thyroid and mammary tissues following iodine exposure. Molecular iodine can increase 6-IL formation in tumor tissue containing elevated arachidonic acid.

Function: 6-Iodolactone is a bioactive iodolipid that mediates part of the antiproliferative and apoptotic effects of iodine. It acts as an activator of PPARγ and can regulate proliferation, differentiation, mitochondrial apoptosis, migration, and tumor-associated signaling.

Cancer: Preclinical studies demonstrate inhibition of tumor-cell proliferation and migration and induction of apoptosis. 6-IL activates PPARγ, and inhibition or knockdown of PPARγ substantially reduces its antiproliferative and pro-apoptotic effects. Antitumor activity has been demonstrated particularly in breast, thyroid, and prostate cancer models.
Scientific Papers found: Click to Expand⟱
7676- iod,    Antineoplastic effect of iodine in mammary cancer: participation of 6-iodolactone (6-IL) and peroxisome proliferator-activated receptors (PPAR)
- in-vivo, BC, NA
TumCP↓, Studies in mammary cancer demonstrated that moderately high concentrations of molecular iodine (I2) have a antiproliferative and apoptotic effect either in vivo as in vitro
Apoptosis↑,
Dose↝, Virgin Sprague-Dawley rats were treated with methyl-nitrosourea (MNU: single dose ip, 50 mg/Kg bw)
other↑, tumoral but not normal mammary tissue contained an elevated basal concentration of AA and significantly more AA-iodinated called 6-iodolactone (6-IL) after chronic I2 treatment.
BloodF↓, Tumors from I2-treated rats showed fewer cells positive to proliferating cell nuclear antigen, lower blood vessel density, as well as decreases in vascular endothelial growth factor, urokinase-type plasminogen activator, and PPAR type alpha (PPARα).
VEGF↓,
UroPA↓,
PPARα↓,
DR4↑, These same tumors showed increases in the cell death markers, TUNEL-positive cells (p < 0.05) and the enzyme caspase-3 (trend), as well as significant induction of PPAR type gamma (PPARγ).
Casp3↑,
PPARγ↑,
antiNeop↑, Together, these data demonstrate that the antineoplasic effect of iodine involves 6-IL formation and PPARγ induction.
Risk↓, Cancer incidence was 37.5% lower in I2-treated than in control rats, whereas the number of tumors per rat and latency were similar for all groups
6IL↑,

7677- iod,    Activation of peroxisome proliferator-activated receptor gamma is crucial for antitumoral effects of 6-iodolactone
- in-vitro, BC, MCF7
TumCP↓, Molecular iodine (I2) exhibits antiproliferative and apoptotic effects on in vivo and in vitro cancer models.
6IL↑, These effects are thought to be mediated by an iodinated arachidonic acid derivative, 6-iodolactone (6IL), and one of the proposed mechanisms is that 6IL activates Peroxisome Proliferator-Activated Receptors type gamma (PPARG).
PPARγ↑,
AntiCan↑, These results support the previously proposed mechanism, in which the I2 effects are mediated by 6IL, and they provide further support for the use of I2 as coadjuvant in breast cancer treatment.

7678- iod,    Signaling pathways involved in the antiproliferative effect of molecular iodine in normal and tumoral breast cells: evidence that 6-iodolactone mediates apoptotic effects
- in-vitro, Nor, MCF12A - in-vitro, BC, MCF7
TumCCA↑, Low-to-moderate concentrations of I(2) (10-20 microM) cause G1 and G2/M phase arrest in MCF-12F and caspase-dependent apoptosis in MCF-7 cells.
selectivity↑, In normal cells, only high doses of I(2) (40 microM) induced apoptosis, and this effect was mediated by poly (ADP-ribose) polymerase-1 (PARP1) and the apoptosis-induced factor, suggesting an oxidative influence of iodine at high concentrations.
6IL↑, Our data indicate that both I(2) and 6-IL trigger the same intracellular pathways and suggest that the antineoplasic effect of I(2) in mammary cancer involves the intracellular formation of 6-IL.
eff↑, Mammary cancer cells are known to contain high concentrations of AA, which might explain why I(2) exerts apoptotic effects at lower concentrations only in tumoral cells.


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

6IL↑, 3,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PPARα↓, 1,   PPARγ↑, 2,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Casp3↑, 1,   DR4↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 2,   UroPA↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,   eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BloodF↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   antiNeop↑, 1,   Risk↓, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: 6IL, 6-Iodolactone
3 iodine
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#:1680  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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