Vitamin K2 / cJun Cancer Research Results

VitK2, Vitamin K2: Click to Expand ⟱
Features:
Vitamin K2 (menaquinone)
Menaquinone-4 (MK-4), a subtype of vitamin K2 Helps blood clot, calcium metabolise and heart health.
Bone health: Vitamin K2 helps to regulate calcium levels in the body, which can help to prevent conditions such as osteoporosis and fractures.
Vitamin K2 has been studied for its potential role in cancer prevention and treatment. Some of the key findings include:
-Shown to inhibit the growth of cancer cells, including those found in leukemia, lung cancer, and prostate cancer.
-Shown to induce apoptosis (cell death) in cancer cells, which can help to prevent the spread of cancer.
-Shown to have anti-angiogenic effects, which means it can help to prevent the formation of new blood vessels that feed cancer cells.
-Synergistic effects with other nutrients, such as vitamin D and calcium, to enhance its anti-cancer effects.

UBIAD1 is the enzyme that makes MK-4 inside tissues

Vitamin K2 exists in several forms known as menaquinones, with MK-4 and MK-7 being the most studied. MK-4 is often used in Japan for therapeutic purposes, whereas MK-7 (derived from bacterial fermentation) is widely available as a supplement in Western countries.
For bone and cardiovascular health—and by extension, exploring potential anticancer benefits—doses for MK-7 commonly range from 90 to 200 micrograms per day.
cJun, cellular Transcription factor Jun: Click to Expand ⟱
Source:
Type: Oncogene
Transcription factor Jun is a protein that in humans is encoded by the JUN gene.
Increased c-jun gene and c-Jun protein expression, and stimulation of c-Jun phosphorylation has been noted under a variety of conditions. Most important member of the AP-1 transcription factor family.
Scientific Papers found: Click to Expand⟱
1817- VitK2,    Research progress on the anticancer effects of vitamin K2
- Review, Var, NA
TumCCA↑, involving cell-cycle arrest
Apoptosis↑, apoptosis, autophagy and invasion
TumAuto↑,
TumCI↓,
TumCG↓, inhibit the growth of cancer cells
ChemoSen↓, combination treatment of VK2 and established chemotherapeutics may achieve better results, with fewer side effects
ChemoSideEff↓,
toxicity∅, VK2 is milder, but causes no side effects, whereas VK1 has the least strong function
Synergy↑, combination of VK2 and vitamin E suppressed the growth of the primary tumor and obliterated the intraperitoneal dissemination in a 65-year-old man with ruptured HCC
cycD1/CCND1↓, decreases in cyclin D1 and cyclin-dependent kinase 4 (CDK4) levels
CDK4↓,
eff↑, pretreatment with VK2 prior to sorafenib treatment is proven to exert more effective HCC growth inhibition in animals than treatment with either alone
IKKα↓, VK2 can inhibit the IκB kinase (IKK)/IκB/NF-κB pathway
NF-kB↓,
other↑, stimulate the phosphorylation of PKA and activate activating protein 2 (AP-2)
p27/CDKN1B↑, VK2 upregulates the expression of p27
cMyc↓, 5 µΜ VK2 exposure inhibited c-MYC expression in HL-60 leukemia cells
i-ROS↑, VK2 treatment increased the intracellular level of the reactive oxygen species (ROS)
Bcl-2↓, VK2 decreases Bcl-2 expression and increases the expression of Bcl-2-associated X protein (Bax)
BAX↑,
p38↑, VK2 activates p38 MAPK to its phosphorylated form
MMP↓, mitochondrial membrane potential was depolarized and caspase-9 was activated
Casp9↑,
p‑ERK↓, VK2 is reported to inhibit ERK phosphorylation by suppressing Ras activation
RAS↓,
MAPK↓, subsequently suppressing the activation of MAPK kinase (MEK)
p‑P53↑, VK2 stimulated the extrinsic apoptosis pathway by increasing p53 phosphorylation
Casp8↑, caspase-8 activation and further activates caspase-3
Casp3↑,
cJun↑, increasing the expression of c-JUN and c-MYC;
MMPs↓, downregulating the expression of matrix metalloproteinases (MMPs)
Synergy↑, combination of VK2 with other chemotherapy agents can produce stronger effects than the use of either alone
Synergy↑, combination of vitamin D3 with VK2 on cancer cells can synergistically improve the induction of cellular differentiation and also significantly reduces the risk of hypercalcemia and vascular calcification


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:


Redox & Oxidative Stress(tgid=1) ⓘ

i-ROS↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   p38↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

p‑ERK↓, 1,   IKKα↓, 1,   MAPK↓, 1,   RAS↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↑, 1,   cMyc↓, 1,   other↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

p‑P53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   p27/CDKN1B↑, 1,   TumCCA↑, 1,  

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

TumCG↓, 1,  

Migration(tgid=13) ⓘ

MMPs↓, 1,   TumCI↓, 1,  

Barriers & Transport(tgid=15) ⓘ

MMP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↓, 1,   eff↑, 1,   Synergy↑, 3,  

Functional Outcomes(tgid=23) ⓘ

ChemoSideEff↓, 1,   toxicity∅, 1,  
Total Targets: 31

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: cJun, cellular Transcription factor Jun
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#:168  Target#:34  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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