VitK3, VitK3,menadione: Click to Expand ⟱
Features:
Menadione (2-methyl-1,4-naphthoquinone, also termed vitamin K3)
Menadione-induced ROS generation is concentration-dependent and high concentrations trigger cell death.
Clinical trials conducted on patients with prostate cancer showed that ascorbic acid-menadione produced an immediate drop in tumor cell numbers through a mechanism named autoschizis.
Scientific Papers found: Click to Expand⟱
2187- SK,  VitK3,    Shikonin, vitamin K3 and vitamin K5 inhibit multiple glycolytic enzymes in MCF-7 cells
- in-vitro, BC, MCF-7
Glycolysis↓, naphthaquinones, including shikonin, vitamin K3 and vitamin K5, have been proven to decrease the rate of glycolysis in cancer cells, which is partly due to suppressed pyruvate kinase activity.
PKM2↓,

609- VitC,  ALA,  VitK3,  Se,    Vitamin C and Cancer: Is There A Use For Oral Vitamin C?
OS↑,

612- VitC,  VitK3,    Effects of sodium ascorbate (vitamin C) and 2-methyl-1,4-naphthoquinone (vitamin K3) treatment on human tumor cell growth in vitro. I. Synergism of combined vitamin C and K3 action
H2O2↑,

635- VitC,  VitK3,    The combination of ascorbate and menadione causes cancer cell death by oxidative stress and replicative stress
- in-vitro, NA, NA
RNR↓, VC/VK3 inhibited RNR mainly by targeting its R2 subunit
GSH↓,
Trx1↓, increased highly oxidized Trx1 (oxidized (and generally less active) means effectively less)
GPx↓, VC/VK3 inhibited glutathione peroxidase activity and led to an elevated level of lipid peroxidation, which triggered apoptosis-inducing factor (AIF) mediated cell death pathway.
lipid-P↑,
AIF↑, which triggered apoptosis-inducing factor (AIF) mediated cell death pathway
ROS↑,

600- VitC,  VitK3,    Serum markers variation consistent with autoschizis induced by ascorbic acid-menadione in patients with prostate cancer
- in-vitro, NA, NA
autoS↑,
TumCD↑,

1819- VitC,  VitK3,    The association of vitamins C and K3 kills cancer cells mainly by autoschizis, a novel form of cell death. Basis for their potential use as coadjuvants in anticancer therapy
- Review, Var, NA
Dose?, coadministration of these vitamins (in a ratio of 100:1, for C and K(3), respectively) produced selective cancer cell death.
TumCD↑,
selectivity↑,
H2O2↑, formation of H(2)O(2) during vitamins redox cycling, oxidative stress, DNA fragmentation
ROS↑,
DNAdam↑,

1836- VitC,  VitK3,  Chemo,    Vitamins C and K3: A Powerful Redox System for Sensitizing Leukemia Lymphocytes to Everolimus and Barasertib
- in-vitro, AML, NA
tumCV↓, Combined administration of 300 μM vitamin C plus 3 μM pro-vitamin K3 reduced the viability of leukemia lymphocytes by ~20%,
selectivity↑, but did not influence the viability of normal lymphocytes
Apoptosis↑, strong induction of apoptosis
eff↑, Leukemia lymphocytes were more sensitive to combined administration of anticancer drug (everolimus or barasertib) plus vitamins C and K3, compared to normal lymphocytes.
ChemoSen↑, combination of vitamin C plus K3 seems to be a powerful redox system that could specifically influence redox homeostasis of leukemia cells and sensitize them to conventional chemotherapy.

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

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

2428- VitK3,    Vitamin K3 and K5 are inhibitors of tumor pyruvate kinase M2
- Study, Var, NA
PKM2↓, VK3 and VK5 showed a significantly stronger potency to inhibit PKM2 than to inhibit PKM1
ChemoSen↑, This study combined with previous reports supports that VK3 and VK5 have potential as adjuvant for cancer chemotherapy.

2372- VitK3,    The role of pyruvate kinase M2 in anticancer therapeutic treatments
- Review, Var, NA
PKM2↓, Chen et al (61) discovered that VK3 and 5 inhibit PKM2 significantly more than PKM1 and pyruvate kinase isoenzyme L, while other isoforms of PK are predominantly expressed in most adult tissues and the liver.
eff↑, demonstrated that combination therapy with VK3 and vitamin C exerts a synergistic anticancer effect in Jurkat and K562 cells
AntiCan↑, Numerous studies have suggested that VK3 and 5 are promising anticancer adjuvants

1839- VitK3,    Vitamin K3 derivative inhibits androgen receptor signaling in targeting aggressive prostate cancer cells
- in-vitro, Pca, NA
TumCP↓, VK3-OCH3 significantly inhibits the proliferation of both RC77-T and MDA-PCa-2b African American PCa cells and promotes apoptosis
Apoptosis↑,
TumCCA↑, blocking the cell cycle at G0
ROS↑, associated with the production of free radicals, such as intracellular and mitochondrial reactive oxygen species (ROS)
eff↓, antioxidants such as N-Acetylcysteine (NAC) and Glutathione (GSH) effectively negated the oxidative stress induced by VK3-OCH3 on PCa cell lines
AR↓, VK3-OCH3 reduces the expression of androgen receptor, TRX2, and anti-apoptotic signaling molecules such as Bcl-2 and TCTP
Trx↓,
Bcl-2↓,

1838- VitK3,  PDT,    Photodynamic Effects of Vitamin K3 on Cervical Carcinoma Cells Activating Mitochondrial Apoptosis Pathways
- in-vitro, Cerv, NA
eff↑, vitamin K3 (Vit K3) serves as a photosensitizer to produce Reactive Oxygen Species (ROS)
ROS↑,
tumCV↓, Vit K3 treatment plus UVA reduced tumor cell viability
TumCG↓, Vit K3 treatment plus UVA can inhibit tumor growth
Apoptosis↑, enhance the apoptosis of cervical cancer cells
cl‑Casp3↑, cleaved caspase-3, cleaved caspase-9, B-cell lymphoma- extra large (Bcl-xl), and cytochrome c (cyt-c) increased obviously,
cl‑Casp9↑,
Bcl-xL↑,
Cyt‑c↑,
Bcl-2↓, (Bcl-2) decreased

1837- VitK3,  VitC,    Alpha-Tocopheryl Succinate Inhibits Autophagic Survival of Prostate Cancer Cells Induced by Vitamin K3 and Ascorbate to Trigger Cell Death
- in-vivo, Pca, NA
eff↑, the combination of α-TOS, VK3 and AA was more efficient in tumor suppression than when the drugs were given separately, without deleterious side effects.
ROS↑, The generation of ROS, cellular response to oxidative stress, and autophagy were investigated in PC3 prostate cancer cells by using drugs at sub-toxic doses.
TumAuto↑, ROS can induce autophagy

1835- VitK3,  VitC,    Potential therapeutic application of the association of vitamins C and K3 in cancer treatment
- Review, Var, NA
ROS↑, A large body of evidence supports the idea that oxidative stress induced by redox cycling of vitamins C and K(3) in association surpasses cancer cellular defense systems and results in cell death
TumCD↑,
TumCG↓, Combined vitamin C and K(3) administration in vitro and in vivo produced tumor growth inhibition and increased the life-span of tumor-bearing mice.
OS↑,

1834- VitK3,  PDT,    Effects of Vitamin K3 Combined with UVB on the Proliferation and Apoptosis of Cutaneous Squamous Cell Carcinoma A431 Cells
- in-vitro, Melanoma, A431
eff↑, co-treatment of VitK3 combined with UVB more significantly inhibited the growth and proliferation of A431 cells than either VitK3 or UVB alone.
TumCG↓,
TumCP↓,
ROS↑, ROS and the depolarization of the mitochondrial membrane potential were higher in all the co-treatment groups
MMP↓,

1832- VitK3,  VitC,    Vitamin K3 and vitamin C alone or in combination induced apoptosis in leukemia cells by a similar oxidative stress signalling mechanism
- in-vitro, AML, K562
ROS↑, vitamin K3- or vitamin C- induced apoptosis in leukemia cells by oxidative stress
H2O2↑, hydrogen peroxide generation,
NF-kB↑, activation of NF-κB,
P53↑, p53, c-Jun, protease caspase-3 activation
cJun↑,
Casp3↑,
MMP↓, mitochondria depolarization leading to nuclei fragmentation
DNAdam↑,
Dose?, Jurkat and K562 cells are exposed to VC and VK3 in a ratio 1000:1 (10 mM: 10 μM) or 100:1 (300 μM: 3 μM), respectively

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.

1828- VitK3,  VitC,    Pankiller effect of prolonged exposure to menadione on glioma cells: potentiation by vitamin C
- in-vivo, GBM, NA
eff↑, menadione:vitamin C at a ratio 1:100 showed higher anti-proliferative activity when compared to each drug alone and allowed to reduce each drug concentration between 2.5 to 5-fold.
ROS↑, cytotoxic effect of menadione is related to the generation of reactive oxygen species
Dose∅, When used in combination at relatively low doses (M:VC at 10 μM:1 mM) for one week M:VC was able to prevent regrowth

1827- VitK3,    A biophysical approach to menadione membrane interactions: relevance for menadione-induced mitochondria dysfunction and related deleterious/therapeutic effects
- Analysis, Var, NA
ROS↑, Menadione (MEN), a polycyclic aromatic ketone, was shown to promote cell injury by imposing massive oxidative stress
ChemoSen↑, has been proposed as a promising chemotherapeutic agent for the treatment of cancer diseases.

1826- VitK3,    PRX1 knockdown potentiates vitamin K3 toxicity in cancer cells: a potential new therapeutic perspective for an old drug
- in-vitro, Cerv, HeLa - in-vitro, Lung, A549
eff↑, PRX1 knockdown in HeLa and A549 cells conferred enhanced sensitivity to vitK3, reducing substantially the necessary doses to kill cancer cells.
ROS↑, Increased ROS accumulation had a crucial role in vitK3-induced cell death in PRX1 knockdown cells.

1821- VitK3,    Menadione (Vitamin K3) induces apoptosis of human oral cancer cells and reduces their metastatic potential by modulating the expression of epithelial to mesenchymal transition markers and inhibiting migration
- in-vitro, Oral, NA - in-vitro, Nor, HEK293 - in-vitro, Nor, HaCaT
selectivity↑, menadione is more cytotoxic to SAS (oral squamous carcinoma) cells but not to non-tumorigenic HEK293 and HaCaT cells.
TumCD↓,
BAX↑, increased the expression of pro-apoptotic proteins, Bax and p53
P53↑,
Bcl-2↓, concurrent decrease in anti-apoptotic proteins, Bcl-2 and p65
p65↓,
E-cadherin↑, Menadione induced the expression of E-cadherin
EMT↓, but reduced the expression of EMT markers, vimentin and fibronectin
Vim↓,
Fibronectin↓,
TumCG↓, Menadione also inhibited anchorage independent growth and migration in SAS cells.
TumCMig↓,

1820- VitK3,    Vitamin K3 (menadione) suppresses epithelial-mesenchymal-transition and Wnt signaling pathway in human colorectal cancer cells
- in-vitro, CRC, SW480 - in-vitro, CRC, SW-620
selectivity↑, Menadione showed cytotoxicity against human CRC cells (SW480 and SW620) and human primary colon cancer cells but was relatively ineffective against the cells from human normal colon (CRL-1790)
TumCI↓, Menadione suppressed invasion, migration and epithelial-mesenchymal transition in human CRC cells
TumCMig↓,
EMT↓,
E-cadherin↑, by upregulating the expression of E-cadherin (CDH1), ZO-1
ZO-1↑,
N-cadherin↓, and downregulating that of N-cadherin (CDH2), Vimentin (VIM), ZEB1, MMP2 and MMP9.
Vim↓,
Zeb1↓,
MMP2↓,
MMP9↓,
TOPflash↓, Menadione decreased TOPFlash/FOPFlash luciferase activity
β-catenin/ZEB1↓, β-catenin (CTNNB1), TCF7L2, Bcl9l, p300 (EP300) and cyclin D1 (CCND1) was suppressed
p300↓,
cycD1↓,
TumCCA↑, SubG0 phase of cell cycle

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: 24

Results for Effect on Cancer/Diseased Cells:
AIF↑,1,   AntiCan↑,2,   Apoptosis↑,3,   AR↓,1,   autoS↑,1,   BAX↑,1,   Bcl-2↓,3,   Bcl-xL↑,1,   BMD↑,1,   Casp3↑,2,   cl‑Casp3↑,1,   cl‑Casp9↑,1,   ChemoSen↑,4,   cJun↑,1,   cycD1↓,1,   Cyt‑c↑,1,   DNAdam↑,2,   Dose?,2,   Dose∅,2,   E-cadherin↑,2,   eff↓,1,   eff↑,8,   EMT↓,2,   Fibronectin↓,1,   Glycolysis↓,1,   GPx↓,1,   GSH↓,1,   H2O2↑,3,   lipid-P↑,1,   MMP↓,2,   MMP2↓,1,   MMP9↓,1,   N-cadherin↓,1,   NF-kB↑,1,   OS↑,2,   p300↓,1,   P53↑,2,   p65↓,1,   PKM2↓,3,   RNR↓,1,   ROS↑,12,   selectivity↑,4,   TOPflash↓,1,   Trx↓,1,   Trx1↓,1,   TumAuto↑,1,   TumCCA↑,3,   TumCD↓,1,   TumCD↑,3,   TumCG↓,4,   TumCI↓,1,   TumCMig↓,2,   TumCP↓,3,   tumCV↓,2,   Vim↓,2,   Zeb1↓,1,   ZO-1↑,1,   β-catenin/ZEB1↓,1,  
Total Targets: 58

Results for Effect on Normal Cells:
Dose↝,1,  
Total Targets: 1

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