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.

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.
Scientific Papers found: Click to Expand⟱
652- EGCG,  VitK2,  CUR,    Case Report of Unexpectedly Long Survival of Patient With Chronic Lymphocytic Leukemia: Why Integrative Methods Matter
- Case Report, CLL, NA
Remission↑, patient has remained asymptomatic for more than 15 years

1211- VitK2,    Mechanisms of PKC-Mediated Enhancement of HIF-1α Activity and its Inhibition by Vitamin K2 in Hepatocellular Carcinoma Cells
- in-vitro, HCC, HUH7
Hif1a↓,
PKCδ↓, protein kinase C (PKC)

2285- VitK2,    New insights into vitamin K biology with relevance to cancer
- Review, Var, NA
Risk↓, Vitamin K intake has been inversely associated with cancer incidence and mortality in observational studies
AntiCan↑, MK4 supplementation on bone loss in women with viral liver cirrhosis.Over 8 years of follow-up, the risk ratio for the development of HCC in the MK4 group compared with the control group was 0.20
eff↑, phase 2 randomized placebo-controlled trial in HCC patients demonstrated that MK4 supplementation (45 mg/day orally) enhanced the efficacy of the multi-kinase inhibitor sorafenib
MMP↓, MK4 mediated apoptosis may also involve binding of MK4 to pro-apoptotic BAK, direct effects on mitochondrial membrane depolarization and reactive oxygen species (ROS)
ROS↑,
Cyt‑c↑, MK4 covalently bound to BAK induces decrease in MMP and cytochrome c release.
eff↓, ROS production can be blocked by N-acetyl-cysteine (NAC) and alpha-tocopherol which can ultimately block MK4 mediated apoptosis.
SXR↑, Activation of SXR by MK4 (The loss of UBIAD1 in prostate cancer cells reduced MK4 synthesis which in turn decreased SXR transcriptional regulation)

2284- VitK2,    Menadione-induced DNA damage in a human tumor cell line
- in-vitro, BC, MCF-7
DNAdam↑, Recently obtained data suggest that the DNA damage in MD-treated MCF-7 cells is directly related to redox cycling and the production of ROS
ROS↑,

2283- VitK2,    Vitamin K Contribution to DNA Damage—Advantage or Disadvantage? A Human Health Response
- Review, Var, NA
*ER Stress↓, protective effect of vitamin K on blood vessels, by reducing inflammation and stress ER
*toxicity↓, Natural forms of vitamin K–K1 and K2—have only a low potential for toxicity
*toxicity↑, However, K3 may demonstrate harmful potential: synthetic vitamin K3 can lead to liver damage
ROS↑, Like another quinone, doxorubicin, menadione exerts its cytotoxic effects by stimulating the generation of oxidative stress, leading to DNA damage
PI3K↑, In bladder cancer cells (T24), vitamin K2 significantly induces PI3K/Akt phosphorylation and increases expression of HIF-1α, intensifying glucose consumption and lactate formation.
Akt↑,
Hif1a↑,
GlucoseCon↑,
lactateProd↑,
ChemoSen↑, Numerous studies indicate that the K vitamins have an additive or synergistic effect on various chemotherapeutic agents.
eff↑, A strong synergism between K1 and sorafenib has been demonstrated in numerous studies
eff↑, ascorbic acid (AA), has a synergistic effect on K3 [73,122,123]. The AA/K3 association leads to an excessive increase in oxidative stress and a decrease in the potential of the mitochondrial membrane, which is a crucial trigger of tumor cell death

2282- VitK2,    Vitamin K prevents oxidative cell death by inhibiting activation of 12-lipoxygenase in developing oligodendrocytes
- in-vitro, Nor, NA
*ROS↓, vitamin K at nanomolar concentrations prevents arachidonic acid-induced oxidative injury to pre-OLs through blocking the activation of 12-lipoxygenase (12-LOX).
*12LOX↓,

2281- VitK2,    The biological responses of vitamin K2: A comprehensive review
- Review, Var, NA
*ROS↓, VitK1 and MK-4 prevent oxidative cell death by blocking the activation of 12-LOX and ROS generation
*12LOX↓,
*NF-kB↓, VitK2 modulates osteoblast and osteoclast formation and activity via downregulation of basal and cytokine-induced NF-κB activation
*BMD↑, strengthens bone construction
*hepatoP↑, VitK2 significantly increased serum albumin levels with concurrent reduction of the levels of alanine and aspartate aminotransferases, suggesting that VitK2 enhances liver regeneration.
cycD1↓, figure 5
PKCδ↓,
STAT3↓,
ERK↑,
MAPK↓,
ROS↑,
PI3K↝,
Akt↝,
Hif1a↝,
*neuroP↑, An increasing body of evidence suggests the possible role of VitK supplementation as a novel neuroprotective strategy in the maintenance of nerve integrity and normal brain function, including cognition and behavior

2280- VitK2,    Vitamin K2 induces non-apoptotic cell death along with autophagosome formation in breast cancer cell lines
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468 - in-vitro, AML, HL-60
ROS↑, ROS production by VK2 seems to be located up-stream in the molecular machinery for both the types of cell death execution
p62↓, decreased expression of p62, a substrate of autophagy, was observed during the exposure to VK2
eff↓, In the presence of NAC and melatonin, the cytotoxic effect by VK2 was significantly suppressed in both cell lines.

2279- VitK2,    Vitamin K2 Induces Mitochondria-Related Apoptosis in Human Bladder Cancer Cells via ROS and JNK/p38 MAPK Signal Pathways
- in-vitro, Bladder, T24 - in-vitro, Bladder, J82 - in-vitro, Nor, HEK293 - in-vitro, Nor, L02 - in-vivo, NA, NA
MMP↓, Vitamin K2 induced apoptosis in bladder cancer cells through mitochondria pathway including loss of mitochondria membrane potential, cytochrome C release and caspase-3 cascade.
Cyt‑c↑,
Casp3↑,
p‑JNK↑, phosphorylation of c-Jun N-terminal kinase (JNK) and p38 MAPK was detected in Vitamin K2-treated cells
p‑p38↑,
ROS↑, generation of reactive oxygen species (ROS) was detected in bladder cancer cells, upon treatment of vitamin K2
eff↓, the anti-oxidant N-acetyl cysteine (NAC) almost blocked the Vitamin K2-triggered apoptosis
tumCV↓, Vitamin K2 significantly decreased the viability of human bladder cancer T24, J82 and EJ cells in a dose- and time-dependent manner
selectivity↑, On the other hand, viability of human normal cells (L02 and HEK293) was minimally affected after exposed to high concentration (100 μM) of Vitamin K2
*toxicity↓,
TumVol↓, in nude mice, vitamin K2 remarkably inhibited the tumor growth and the tumor volume was gradually reduced after the 11th day, compared with the sustained growth of control group.

2278- VitK2,  VitK3,  VitC,    Vitamin K: Redox-modulation, prevention of mitochondrial dysfunction and anticancer effect
- Review, Var, NA
ChemoSen↑, The analyzed data suggest that vitamin C&K can sensitize cancer cells to conventional chemotherapy, which allows achievement of a lower effective dose of the drug and minimizing the harmful side-effects.
ROS↑, modulation of redox-balance and induction of oxidative stress in cancer cells due to quinone structure of vitamin K.
eff↑, Vitamin C plus K3: A powerful redox-system to sensitize cancer cells towards chemotherapeutics

2277- VitK2,    Vitamin K2 suppresses rotenone-induced microglial activation in vitro
- in-vitro, Nor, BV2 - NA, AD, NA - NA, Park, NA
*p38↓, MK-4 (5–20 μmol/L) significantly inhibited rotenone-induced p38 activation, ROS production, and caspase-1 activation in BV2 cells
*ROS↓,
*Casp1↓,
*MMP↑, MK-4 (5–20 μmol/L) also restored the mitochondrial membrane potential that had been damaged by rotenone
*NF-kB↓, inhibiting NF-κB activation
*IL1β↓, MK-4 suppresses rotenone-induced activation of NF-κB and the production of inflammatory factors, including TNF-α, IL-1β, iNOS and COX-2
*iNOS↓, fig1
*COX2↓, fig1
*TNF-α↓, fig1

2276- VitK2,    Vitamin K2 (MK-7) Intercepts Keap-1/Nrf-2/HO-1 Pathway and Hinders Inflammatory/Apoptotic Signaling and Liver Aging in Naturally Aging Rat
- in-vivo, Nor, NA
*Albumin↑, parallel significant restoration of the serum total protein and albumin by 1.1- and 1.13-fold
*AST↓, VK2 administration reversed this situation, as confirmed by the significant decrease in serum ALT and AST by 0.25- and 0.27-fold
*ALAT↓,
*Keap1↓, significant decrease in Keap-1 mRNA by 0.32-fold
*NRF2↑, significant restoration of the Nrf-2 mRNA level
*HO-1↑,
*COX2↓, VK2 administration to aged animals attenuated hepatic inflammation where hepatic sections from aged-treated rats demonstrated a marked downregulation in COX-2, iNOS and TNF-α
*iNOS↓,
*TNF-α↓,
*TIMP1↓, VK2-treated aged rats showed a significant downregulation in both hepatic TIMP-1 concentration and TGF-β immunostaining compared to the aged untreated control
*TGF-β↓,
*ROS↓, Emerging evidence reported Nrf-2 signaling and VK to play a crucial role in counteracting oxidative stress, DNA damage, senescence and inflammation. These events help in quenching ROS
*DNAdam↓,
*Inflam↓,

2275- VitK2,    Delivery of the reduced form of vitamin K2(20) to NIH/3T3 cells partially protects against rotenone induced cell death
- in-vitro, Nor, NIH-3T3
*MMP↓, MK-4 and MKH derivatives suppressed cell death, the decline in mitochondrial membrane potential (MMP), excessive reactive oxygen species (ROS) production, and a decrease in intrinsic coenzyme Q9 (CoQ9) induced by rotenone (ROT, complex I inhibitor).
*ROS↓, MK-4 and MKH derivatives suppress ROT-induced ROS
*HO-1↓, MK-4 and MKH derivatives suppress ROT-induced heme oxygenase-1 expression. HO-1 protein expression was clearly increased by ROT

2274- VitK2,    Vitamin K2 Modulates Mitochondrial Dysfunction Induced by 6-Hydroxydopamine in SH-SY5Y Cells via Mitochondrial Quality-Control Loop
- in-vitro, Nor, SH-SY5Y
*Bcl-2↓, Vitamin K2 played a significant part in apoptosis by upregulating and downregulating Bcl-2 and Bax protein expressions, respectively, which inhibited mitochondrial depolarization, and ROS accumulation to maintain mitochondrial structure and function
*BAX↑,
*MMP↑, vitamin K2 can restore the mitochondrial membrane potential and inhibit mitochondrial depolarization caused by 6-OHDA.
*ROS↓, vitamin K2 can effectively remove the ROS generated by 6-OHDA and relieve cellular oxidative stress.
*p62↓, vitamin K2 treatments downregulated the expression level of p62 and upregulated the expression level of LC3A
*LC3A↑,
*Dose↝, vitamin K2 inhibited the toxic effect of 6-OHDA, and that the inhibitory effect was the best at a concentration of 30 µM
*Apoptosis↓, However, after vitamin K2 post-treatment, the apoptosis rate was significantly reduced to 11.44%.
*PINK1↑, Vitamin K2 Regulates Mitochondrial Quality-Control System by Activating Pink1/Parkin Signaling Pathway
*PARK2↑,

1840- VitK2,    The mechanisms of vitamin K2-induced apoptosis of myeloma cells
- in-vitro, Melanoma, NA
TumCG↓, growth inhibition was caused by apoptosis and activation of caspase-3
Apoptosis↑,
Casp3↑,
ROS↑, generation of superoxide
p‑MAPK↑, phosphorylation of MAPK was increased by VK2

1833- VitK2,    Divergent effects of vitamins K1 and K2 on triple negative breast cancer cells
- in-vitro, BC, HS587T - in-vitro, BC, MDA-MB-231 - in-vitro, BC, SUM159
TumCP↓, K2 exposure reduced stemness and elicited anti-proliferative effects
other↑, we hypothesize that in normal breast, K1 is converted to menadione which is prenylated by UBIAD1 to K2, favoring tumor suppression

1830- VitK2,    Vitamin K Intake and Risk of Lung Cancer: The Japan Collaborative Cohort Study
- Study, Lung, NA
Risk↓, Vitamin K consumption reduces the risk of lung cancer.
NF-kB↓, Vitamin K2 has been shown to suppress nuclear factor (NF)-κB activation via inhibiting protein kinase C (PKC)- α and ε kinase activities
PKCδ↓,

1829- VitK2,    Vitamin K: New insights related to senescence and cancer metastasis
- Review, Var, NA
TumCP↓, VK can inhibit the proliferation, growth, and differentiation of cancer cells
TumCG↓,
ChemoSen↑, VK as an adjuvant therapy for cancer (or in combination with traditional chemotherapy drug
ROS↑, VK can regulate the balance of oxidation-reduction reaction(redox) by producing reactive oxygen species (ROS) through the mitochondrial pathway.

1825- VitK2,    Vitamin K intake and prostate cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer (PLCO) Screening Trial
- Analysis, Pca, NA
Risk∅, The present study does not suggest that vitamin K intake influences the occurrence of total and advanced prostate cancer in the general US population

1824- VitK2,    Vitamin K and its analogs: Potential avenues for prostate cancer management
- Review, Pca, NA
AntiCan↑, potential anticancer activity in several cancer types including prostate cancer
toxicity∅, VK1 and VK2 are non-toxic even at high doses
Risk↓, Epidemiological studies suggest that there is inverse association between dietary intake of VK (especially menaquinone) and overall cancer incidence
Apoptosis↑, VK2 has anticancer activity through the mechanisms such as induction of apoptosis, production of reactive oxygen species (ROS) and cell cycle arrest
ROS↑,
TumCCA↑,
eff↑, Gilloteaux et al. [90] reported that the combination of VK3 and ascorbic acid induces oxidative stress in DU-145 PCa cells.
DNAdam↑, oxidative stress induce lipid and protein oxidative modifications and DNA damage leading to apoptotic cell death
MMP↓, VK2 induces pro-apoptosis effects by regulating the MMP, in which mechanism VK2 produces superoxide within the mitochondrial membrane, followed by the release cytochrome c, activation of procaspase 3
Cyt‑c↑,
pro‑Casp3↑,
FasL↑, VK3 treatment induced c-myc and also increased both FasL and Fas
Fas↑,
TumAuto↑, VK2 also can induce autophagy
ChemoSen↑, combination of vitamins C and VK3 has been proposed as a non-toxic mixture of drugs active as an adjuvant cancer therapy by increasing chemo- or radiotherapy effects through alteration of deoxyribonuclease activity
RadioS↑,

1823- VitK2,  VitK3,    Vitamins K2, K3 and K5 exert antitumor effects on established colorectal cancer in mice by inducing apoptotic death of tumor cells
- in-vitro, CRC, NA - in-vivo, NA, NA
TumCP↓, Vitamins K2, K3 and K5 suppressed the proliferation of colon 26 cells
TumCCA↑, population in sub-G1 phase of the cell cycle.
Casp3↑, caspase-3 in colon 26 cells was significantly up-regulated by vitamins K2, K3 and K5

1822- VitK2,    Vitamin K: A novel cancer chemosensitizer
- Review, Var, NA
ChemoSen↑, combination of vitamin K analogs, such as vitamins K1, K2, K3, and K5, with other chemotherapeutic drugs have demonstrated a safe, cost-effective, and most efficient way to overcome drug resistance and improved the outcomes of prevailing chemotherapy
Apoptosis↑, promoting apoptosis and cell cycle arrest and overcoming drug resistance by inhibiting P-glycoprotein.
TumCCA↑,
P-gp↓,

1818- VitK2,    New insights on vitamin K biology with relevance to cancer
- Review, Var, NA
TumCG↓, A few small randomized trials support the concept that vitamin K supplementation can retard cancer development and/or progression
ChemoSen↑, phase 2 randomized placebo-controlled trial in HCC patients demonstrated that MK4 supplementation (45 mg/day orally) enhanced the efficacy of the multi-kinase inhibitor sorafenib
toxicity∅, long term vitamin K supplementation is safe and may offer survival benefit in HCC patients.
OS↑,
BMD↑, Primary Outcomes: Bone density
eff↑, In studies where both forms of the vitamin have been compared, MKs generally exerted more potent anticancer effects than PK.
MMP↓, direct effects on mitochondrial membrane depolarization and reactive oxygen species (ROS)
ROS↑,
eff↓, ROS neutralization by antioxidants (N-acetyl cysteine (NAC) and alpha-tocopherol) or BAK knockdown prevented MK4 mediated mitochondrial disruption and apoptosis
ERK↑, activates ERK, JNK/p38 MAPK
JNK↑,
p38↑,
Cyt‑c↑, cytochrome c release
Casp↑, caspase activation
ATP↓, reducing ATP production and increasing lactate production
lactateProd↑,
AMPK↑, which activates AMPK
Rho↓, via inhibition of RhoA
TumCG↓, mouse xenograft studies, treatment with MK4 administered in water at a calculated dose of 20 mg/kg/d significantly reduced growth of established HCCs
BioAv↑, Phylloquinone (K1) is the major dietary form, but it is converted into menaquinone (K2) in tissues.
cardioP↑, optimal vitamin K status is common in adults and may contribute to chronic diseases such as osteoporosis, type 2 diabetes and cardiovascular disease.
Risk↓, Observational studies suggest that low vitamin K intake increases cancer risk(more lowers risk)

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
eff↑, 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↓, 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↑, 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)
eff↑, combination of VK2 with other chemotherapy agents can produce stronger effects than the use of either alone
eff↑, 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

1816- VitK2,    Role of Vitamin K in Selected Malignant Neoplasms in Women
- Review, Var, NA
TumCP↓, inhibition of proliferation
TumMeta↓, inhibition of the potential for metastasis
TumAuto↑, induction of autophagy or apoptosis
Apoptosis↑,
Apoptosis↑, apoptosis, caspase 3/7 activity, increased levels of reactive oxygen species (ROS),
Casp3↑,
Casp7↑,
ROS↑,
AR↓, decreased androgen receptor expression
EMT↓, Vitamin K3 inhibited the epithelial-mesenchymal transition (EMT) and Wnt
Wnt↓,
MMP↓, vitamin K leads to depolarization of the mitochondrial membrane and a release of cytochrome c into the cytosol
Cyt‑c↑,
NF-kB↓, vitamin K2 can reduce cyclin D1 expression in cancer cells by inhibiting the binding of the nuclear factor κB (NF-κB)
cycD1↓,
TumCCA↓, arresting the cell cycle in the G1 phase

1214- VitK2,    Vitamin K2 promotes PI3K/AKT/HIF-1α-mediated glycolysis that leads to AMPK-dependent autophagic cell death in bladder cancer cells
- in-vitro, Bladder, T24 - in-vitro, Bladder, J82
Glycolysis↑, Vitamin K2 renders bladder cancer cells more dependence on glycolysis than TCA cycle
GlucoseCon↑, results suggest that Vitamin K2 is able to induce metabolic stress, including glucose starvation and energy shortage, in bladder cancer cells, upon glucose limitation.
lactateProd↑,
TCA↓, Vitamin K2 promotes glycolysis and inhibits TCA cycle in bladder cancer cells
PI3K↑,
Akt↑,
AMPK↑, Vitamin K2 remarkably activated AMPK pathway
mTORC1↓,
TumAuto↑,
GLUT1↑, Vitamin K2 stepwise elevated the expression of some glycolytic proteins or enzymes, such as GLUT-1, Hexokinase II (HK2), PFKFB2, LDHA and PDHK1, in bladder cancer T24
HK2↑,
LDHA↑, Vitamin K2 stepwise elevated the expression of some glycolytic proteins or enzymes, such as GLUT-1, Hexokinase II (HK2), PFKFB2, LDHA and PDHK1, in bladder cancer T24
ACC↓, Vitamin K2 remarkably decreased the amounts of Acetyl coenzyme A (Acetyl-CoA) in T24 cells
PDH↓, suggesting that Vitamin K2 inactivates PDH
eff↓, Intriguingly, glucose supplementation profoundly abrogated AMPK activation and rescued bladder cancer cells from Vitamin K2-triggered autophagic cell death.
cMyc↓, c-MYC protein level was also significantly reduced in T24 cells following treatment with Vitamin K2 for 18 hours
Hif1a↑, Besides, the increased expression of GLUT-1, HIF-1α, p-AKT and p-AMPK were also detected in Vitamin K2-treated tumor group
p‑Akt↑,
eff↓, 2-DG, 3BP and DCA-induced glycolysis attenuation significantly prevented metabolic stress and rescued bladder cancer cells from Vitamin K2-triggered AMPK-dependent autophagic cell death
eff↓, inhibition of PI3K/AKT and HIF-1α notably attenuated Vitamin K2-upregulated glycolysis, indicating that Vitamin K2 promotes glycolysis in bladder cancer cells via PI3K/AKT and HIF-1α signal pathways.
eff↓, (NAC, a ROS scavenger) not only alleviated Vitamin K2-induced AKT activation and glycolysis promotion, but also significantly suppressed the subsequent AMPK-dependent autophagic cell death.
eff↓, glucose supplementation not only restored c-MYC expression, but also rescued bladder cancer cells from Vitamin K2-triggered AMPK-dependent autophagic cell death
ROS↑, under glucose limited condition, the increased glycolysis inevitably resulted in metabolic stress, which augments ROS accumulation due to lack of glucose for sustained glycolysis.

1213- VitK2,    Vitamin K2 Inhibits Hepatocellular Carcinoma Cell Proliferation by Binding to 17β-Hydroxysteroid Dehydrogenase 4
- in-vitro, HCC, HepG2
HSD17B4↓, VK2 directly binds to HSD17B4, but does not affect the expression of HSD17B4, to inhibit the proliferation of HCC cells by inhibiting the activation of Akt and MEK/ERK signaling pathways, leading to decreased STAT3 activation
Akt↓,
MEK↓,
ERK↓,
STAT3↓,
TumCP↓,

1212- VitK2,    Vitamin K2 stimulates osteoblastogenesis and suppresses osteoclastogenesis by suppressing NF-κB activation
- in-vitro, ostP, NA
NF-kB↓,

1831- VitK3,  VitK2,    The anticancer effects of vitamin K
- Review, Var, NA
AntiCan↑, considerable research demonstrating an anticancer potential
Dose∅, Much of this research has focused on vitamin K3, although vitamins K2 and K1 have also been shown to have anticancer effects.

1815- VitK3,  VitK2,    Vitamin K
- Review, Nor, NA
*Dose↝, 19+ years - 120 mcg (male) 90 mcg(female)
BMD↑, Some, but not all, studies also link higher vitamin K intakes with higher bone mineral density and/or lower hip fracture incidence


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 30

Results for Effect on Cancer/Diseased Cells:
ACC↓,1,   Akt↓,1,   Akt↑,2,   Akt↝,1,   p‑Akt↑,1,   AMPK↑,2,   AntiCan↑,3,   Apoptosis↑,6,   AR↓,1,   ATP↓,1,   BAX↑,1,   Bcl-2↓,1,   BioAv↑,1,   BMD↑,2,   cardioP↑,1,   Casp↑,1,   Casp3↑,5,   pro‑Casp3↑,1,   Casp7↑,1,   Casp8↑,1,   Casp9↑,1,   CDK4↓,1,   ChemoSen↓,1,   ChemoSen↑,6,   ChemoSideEff↓,1,   cJun↑,1,   cMyc↓,2,   cycD1↓,3,   Cyt‑c↑,5,   DNAdam↑,2,   Dose∅,1,   eff↓,9,   eff↑,10,   EMT↓,1,   ERK↓,1,   ERK↑,2,   p‑ERK↓,1,   Fas↑,1,   FasL↑,1,   GlucoseCon↑,2,   GLUT1↑,1,   Glycolysis↑,1,   Hif1a↓,1,   Hif1a↑,2,   Hif1a↝,1,   HK2↑,1,   HSD17B4↓,1,   IKKα↓,1,   JNK↑,1,   p‑JNK↑,1,   lactateProd↑,3,   LDHA↑,1,   MAPK↓,2,   p‑MAPK↑,1,   MEK↓,1,   MMP↓,6,   MMPs↓,1,   mTORC1↓,1,   NF-kB↓,4,   OS↑,1,   other↑,2,   P-gp↓,1,   p27↑,1,   p38↑,2,   p‑p38↑,1,   p‑P53↑,1,   p62↓,1,   PDH↓,1,   PI3K↑,2,   PI3K↝,1,   PKCδ↓,3,   RadioS↑,1,   RAS↓,1,   Remission↑,1,   Rho↓,1,   Risk↓,4,   Risk∅,1,   ROS↑,13,   i-ROS↑,1,   selectivity↑,1,   STAT3↓,2,   SXR↑,1,   TCA↓,1,   toxicity∅,3,   TumAuto↑,4,   TumCCA↓,1,   TumCCA↑,4,   TumCG↓,5,   TumCI↓,1,   TumCP↓,5,   tumCV↓,1,   TumMeta↓,1,   TumVol↓,1,   Wnt↓,1,  
Total Targets: 94

Results for Effect on Normal Cells:
12LOX↓,2,   ALAT↓,1,   Albumin↑,1,   Apoptosis↓,1,   AST↓,1,   BAX↑,1,   Bcl-2↓,1,   BMD↑,1,   Casp1↓,1,   COX2↓,2,   DNAdam↓,1,   Dose↝,2,   ER Stress↓,1,   hepatoP↑,1,   HO-1↓,1,   HO-1↑,1,   IL1β↓,1,   Inflam↓,1,   iNOS↓,2,   Keap1↓,1,   LC3A↑,1,   MMP↓,1,   MMP↑,2,   neuroP↑,1,   NF-kB↓,2,   NRF2↑,1,   p38↓,1,   p62↓,1,   PARK2↑,1,   PINK1↑,1,   ROS↓,6,   TGF-β↓,1,   TIMP1↓,1,   TNF-α↓,2,   toxicity↓,2,   toxicity↑,1,  
Total Targets: 36

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:168  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page