necrosis Cancer Research Results
necrosis, necrosis: Click to Expand ⟱
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| Type: type of cell death |
Necrosis is a type of cell death that occurs when cells are damaged or injured, leading to the loss of cellular homeostasis and the eventual death of the cell. Necrosis is a non-programmed form of cell death, meaning that it is not a deliberate or controlled process, but rather a response to cellular damage or injury.
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Scientific Papers found: Click to Expand⟱
TrxR↓, Auranofin (Au), an inhibitor of thioredoxin reductase, is a known anti‑cancer drug
AntiCan↑,
TumCG↓, Au inhibited the growth of HeLa cells with an IC50 of ~2 µM at 24 h.
Apoptosis↑, This agent induced apoptosis and necrosis, accompanied by the cleavage of poly (ADP‑ribose) polymerase and loss of mitochondrial membrane potential.
necrosis↑,
cl‑PARP↑,
MMP↓,
ROS↑, With respect to the levels of ROS and GSH, Au increased intracellular O2•- in the HeLa cells and induced GSH depletion.
GSH↓,
eff↓, The antioxidant, N‑acetyl cysteine, not only attenuated apoptosis and necrosis in the Au‑treated HeLa cells, but also decreased the levels of O2•- and GSH depletion in the cells.
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in-vitro, |
AML, |
Jurkat |
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in-vitro, |
Nor, |
L929 |
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necrosis↑, Allicin induces apoptosis or necrosis in a dose-dependent manner but biocompatible doses influence cellular metabolism and signalling cascades.
Thiols↓, Oxidation of protein thiols and depletion of the glutathione pool are thought to be responsible for allicin's physiological effects.
GSH↓,
ENO1↓, allicin caused inhibition of enolase activity, an enzyme considered a cancer therapy target.
Zn2+↑, Allicin leads to Zn2+ release in murine EL-4 cells
Glycolysis↓, suggests that allicin can inhibit glycolysis which provides electron donors for ATP generation required for cellular biosynthesis pathways and growth of the cells.
ATP↓,
BioAv↓, achieving therapeutically relevant concentrations of allicin via the oral route is therefore unlikely and more direct routes of application to the desired site of action need to be considered
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vitro+vivo, |
GBM, |
A172 |
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vitro+vivo, |
GBM, |
U87MG |
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HR↓,
RAD51↓,
Apoptosis↑,
necrosis↑,
ROS↑,
ChemoSen↑, Enhancement of the antitumor effect of TMZ by co-administration of ART was also observed in a mouse tumor model.
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in-vitro, |
Liver, |
HepG2 |
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in-vitro, |
Cerv, |
HeLa |
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Dose↝, The combination of ART and Res exhibited the strongest anticancer effect at the ratio of 1:2 (ART to Res).
TumCMig↓, combination of the two drugs also markedly reduced the ability of cell migration
Apoptosis↑, Apoptosis analysis showed that combination of ART and Res significantly increased the apoptosis and necrosis rather than use singly
necrosis↑,
ROS↑, ROS levels were elevated by combining ART with Res.
eff↑, the data suggested that the IC50 of the combination of ART and Res is lower than that of each drug used alone.
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in-vitro, |
BC, |
MCF-7 |
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in-vitro, |
Nor, |
HUVECs |
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toxicity↝, We have found that baicalin and baicalein demonstrated cytotoxicity towards both cell lines, with more potent effects observed in baicalein.
ChemoSen↑, Both flavonoids, baicalin (167 µmol/L) and baicalein (95 µmol/L), synergistically enhanced the cytotoxic, proapoptotic, and genotoxic activity of doxorubicin and docetaxel in breast cancer cells.
selectivity↑, Surprisingly, low concentrations of baicalin and baicalein had a greater effect on MCF-7 viability. A
Apoptosis↑, Induction of Apoptosis and Necrosis by Baicalin and Baicalein Used alone and in Combination with Anticancer Drugs
necrosis↑,
MMP↓, After treatment with baicalin and baicalein at high concentrations (IC50), the ΔΨm of cancer cells was diminished to 30% of the control value
DNAdam↑, DNA Damage Induced by Baicalin and Baicalein Used Alone and in Combination with Anticancer Drugs
cl‑PARP↑, PARP Cleavage Induced by Baicalin and Baicalein Used Alone and in Combination with Anticancer Drugs
MRP1↓, Moreover, baicalin and baicalein reduced cisplatin resistance by inhibiting the expression of genes involved in drug resistance, such as MRP1 [30] and Bcl-2, and via the Akt/mTOR and Nrf2/Keap 1 pathway [26].
Bcl-2↓,
hepatoP↑, baicalin and baicalein can also help decrease the side effects of cisplatin treatment by protecting the liver from damage [31]
cardioP↑, Similar to baicalein, baicalin also significantly protects against doxorubicin’s cardiotoxicity.
BioAv↝, This is because baicalein has a smaller size and high lipophilicity, contributing to fast absorption and an improved ability to penetrate cells [60].
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in-vitro, |
Melanoma, |
B16-F10 |
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ROS↑,
eff↓, ROS scavengers effectively reversed cell viability reduction induced by baicalein
tumCV↓,
Casp3↑,
necrosis↑,
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in-vitro, |
Melanoma, |
SK-MEL-28 |
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Apoptosis↑,
necrosis↑,
DNAdam↑, increase in the DNA damage index
TumCCA↑, G1/G0 phase
ROS↑, The alcaloid increased (****p < 0.001) ROS production compared to untreated controls with an increase in activated caspase 3 and phosphorylated p53 protein levels
Casp3↑,
p‑P53↑,
ERK↑, BBR significantly enhanced ERK as well as both pro- and anti-inflammatory cytokine expression compared to untreated controls.
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in-vitro, |
CRC, |
HT29 |
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in-vitro, |
CRC, |
SW480 |
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in-vitro, |
CRC, |
HCT116 |
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TumCP↓, We demonstrated that treatment of these CRC cell lines with berberine inhibited cell proliferation, migration and invasion through induction of apoptosis and necrosis.
TumCMig↓,
TumCI↓,
Apoptosis↑,
necrosis↑,
AQPs↓, berberine treatment down-regulated the expression of all three types of AQPs.
PTEN↑, up-regulating PTEN and down-regulating PI3K, AKT and p-AKT expression as well as suppressing its downstream targets, mTOR and p-mTOR at the protein level
PI3K↓,
Akt↓,
p‑Akt↓,
mTOR↓,
p‑mTOR↓,
Apoptosis↑, BJO induced AML cell apoptosis through activation of caspase-8 and modulation of apoptosis-related proteins.
Casp8↑,
TumCCA↑, BJO also increased subG1 phase cells and cause PARP cleavage in AML patients' leukemia cells.
cl‑PARP↑,
eff↝, Moreover, oleic acid and linoleic acid were found to be the active components of BJO.
TumCG↓, Furthermore, intravenous injection of BJO significantly inhibited U937 tumor growth in the xenograft mouse model.
necrosis↑, BJO induced apoptosis at low concentrations and induced necrosis at higher concentrations
Fas↑, upregulating expression of Fas in leukemia cells
TumCCA↑, BJO can arrest the cell cycle in G0/G1 phase [6, 7] to inhibit cell growth.
selectivity↑, Its apoptotic effect on AML cells was much more potent than on normal PBLs from healthy volunteers.
Apoptosis↑, This study revealed that short-term fasting chemotherapy significantly improved HNSCC cell line apoptosis and necrosis.
necrosis↑,
Apoptosis↑,
necrosis↑,
TumAuto↑,
ERK↓, ERK1/2
p38↓,
NF-kB↓,
VEGF↓,
OS↑, A statistically greater overall survival fraction was noted in the high-dose H-FIRE + liposomal doxorubicin
CellMemb↑, defects facilitate an increase in cell membrane permeability
Imm↑, non-thermal cell death mechanism induced by IRE can improve upon the antigen presentation and consequently the immune response
Inflam↓, cell death is in part pro-inflammatory (necrosis and pyroptosis),
necrosis↑,
Pyro↑,
eff↑, H-FIRE utilizes bursts of biphasic pulsed electric fields to non-thermally ablate neoplastic and non-neoplastic tissue while mitigating excitation of skeletal muscle and nerves during tissue ablation.
IL2↑, IFNγ, interleukin-2 (IL-2) (p< 0.01), interleukin-6 (IL-6) (p< 0.01), and interleukin-17a (IL-17a) (p< 0.001) were significantly elevated in rats treated with H-FIRE ablation
IL6↑,
IL17↑,
IFN-γ↓,
other↝, Figure 1, equivalent electrical circuit
ROS↑, Another aspect to consider is the fact that PEF application has been shown to result in reactive oxygen species (ROS) production not only in cells71,72 but also in the medium surrounding the cells
Temp∅, Provided the number of pulses and the PRF are not too high, allowing for interpulse heat dissipation, in most cases, thermal effects can even be neglected.
CellMemb↑, he main primary effect of nsPEFs is the permeabilization of both the cell membrane82 and organelle membranes, followed by calcium entry,83 loss of resting membrane potential,62,84 increased cellular K+ efflux,84 activation of VGCC ion channels
Ca+2↑, In addition to apoptosis, nsPEFs are known to trigger calcium mobilization.
Apoptosis↑, The apoptosis is characterized by several morphological changes in the cell, due to energy-dependent biochemical mechanisms, leading to cell death
TumCD↑,
MMP↓, , while the dissipation of ψ (mitochondria membrane potential) occurs at a higher level (around 40 kV/cm)
necrosis↑, A severe dysregulation of Ca2+ stimulates a cell death by necrosis, while a milder dysregulation provokes a cell death by apoptosis.103
TumVol↓, As a result, tumor shrinkage of 90% could be observed within 2 weeks, and the repetition of a second treatment at that time could result in complete regressions.
Remission↑,
Hif1a↓,
NF-kB↓,
GLUT1↓,
GLUT4↓,
HK2↓,
LDHA↓,
TumCCA↑, G0/G1 cell cycle arrest
TumMeta↓,
GlucoseCon↓, 5%-20% of control for glucose uptake
ATP↓,
necrosis↑, cells incubated with Graviola extract have a gain in cell volume, a characteristic of necrotic cell death
Casp∅, Caspase-3 expression values remained statistically unaltered by treatment with the extract, suggesting that apoptotic pathways are not involved
p‑FAK↓,
MMP9↓,
MUC4↓, significant downregulation in MUC4
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in-vitro, |
CRC, |
HCT116 |
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in-vitro, |
BC, |
MDA-MB-231 |
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Apoptosis↑,
necrosis↑,
TumAuto↑,
HIF-1↓,
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
Nor, |
MCF10 |
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TumCD↑,
necrosis↑, in normal MCF10A cells
mt-ROS↑, ELF-MF significantly increase the mitochondrial reactive oxygen species production in both MCF-10A and MDA-MB-231 cells, compared to the unexposed cell
other↑, ELF-MF exposed MCF-10A cells exhibited 53 upregulated and 189 downregulated proteins compared with control cells while exposed MDA-MB-231 cells showed 242 upregulated and 86 downregulated proteins compared with the control cells.
*STAT3↓, normal cells
STAT3↑, cancer cells
*Inflam↓, common use as an anti-inflammatory agent
*Pain↓, A variety of health-specific outcome measures are improved with MSM supplementation, including inflammation, joint/muscle pain, oxidative stress, and antioxidant capacity.
*ROS↓,
*antiOx↑,
*Dose↝, MSM is well-tolerated by most individuals at dosages of up to four grams daily, with few known and mild side effects
*Half-Life↝, Pharmacokinetic studies indicate that MSM is rapidly absorbed in rats [63,64] and humans [65], taking 2.1 h and <1 h, respectively.
*NF-kB↓, The inhibitory effect of MSM on NF-κB results in the downregulation of mRNA for interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α) in vitro
*IL1↓,
*IL6↓,
*TNF-α↓,
*iNOS↓, MSM can also diminish the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) through suppression of NF-κB;
*COX2↓,
*NLRP3↓, MSM negatively affects the expression of the NLRP3 inflammasome by downregulating the NF-κB production of the NLRP3 inflammasome transcript and/or by blocking the activation signal in the form of mitochondrial generated reactive oxygen species (ROS)
*NRF2↑, MSM influences the activation of at least four types of transcription factors: NF-κB, signal transducers and activators of transcription (STAT), p53, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2).
*STAT↓, MSM has been shown to repress the expression or activities of STAT transcription factors in a number of cancer cell lines in vitro
*Cartilage↑, , in vitro studies suggest that MSM protects cartilage through its suppressive effects on IL-1β and TNF-α
*eff↑, Supplementation with glucosamine, chondroitin sulfate, MSM, guava leaf extract, and Vitamin D improved physical function in patients with knee osteoarthritis based on the Japanese Knee OA Measure
*eff↑, MSM in combination with boswellic acid was also shown to improve knee joint function as assessed through the Lequesne Index
*GSH↑, MSM is able to restore the reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio to normal levels, decrease NO production, and reduce neuronal ROS production following HIV-1 Tat exposure
*uricA↓, Humans studies show promise for MSM as an antioxidant with similar results noted, including reductions in MDA [19,167,168], protein carbonyls (PC) [167,168], and uric acid [168] and increases in GSH [167] and TEAC [159,161,168].
tumCV↓, MSM independently has been shown to be cytotoxic to cancer cells by inhibiting cell viability through the induction of cell cycle arrest [119,122,123], necrosis [119], or apoptosis
TumCCA↑,
necrosis↑,
Apoptosis↑,
VEGF↓, reduced expression of oncogenic proteins such as vascular endothelial growth factor (VEGF) [99,100,101,123], heat shock protein (HSP)90α [100], and insulin-like growth factor-1 receptor (IGF-1R)
HSP90↓,
IGF-1?,
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vitro+vivo, |
BC, |
MDA-MB-231 |
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ChemoSen↑, synergistic interaction between DOX and PIP on MDA-MB-231 cells.
necrosis↑, combination regimen to enhance necrosis while downregulating PTEN and curbing PI3K levels as well as p-Akt, mTOR, and ALDH-1 immunoreactivities.
PTEN↓,
PI3K↓,
p‑Akt↓,
mTOR↓,
ALDH↓,
TumVol↓, Combining PIP to DOX reduces tumor size and improves survival of tumor-bearing mice
OS↑, combining PIP to DOX improved survival rates in mice compared to their DOX-treated counterparts (Fig. 4B).
cardioP↑, PIP protects against DOX-induced cardiotoxicity
cl‑PARP↑, PIP enhances apoptosis via PARP cleavage in EAC-tumor bearing mice
TumCCA↑, They induced apoptotic changes as well as cell cycle arrest at G2/M phase. They enhanced ROS expression in cancer cells
ROS↑, The treatment of cancer cells with RE leads to a strong increase in intracellular ROS that results in cell death.
Bcl-2↓,
BAX↑,
Casp3↑,
P53↑,
necrosis↑, RE in a dose of 20–40 µg/ml resulted in an obvious increase in ROS intracellularly which guided cells toward necrosis and death.
eff↑, Chitosan was chosen as a nanodrug delivery in our research as per our aim, and we intended to offer a locally acting formula that may be applicable in managing oral cancerous lesions. Chitosan has a penetration capability as it is able to open tight
BioAv↑, chitosan nanoparticles, an increase in the surface-to-volume ratio occurs as well as the specific surface area. This enhances the dissolution of poorly water-soluble drugs so increases their bioavailability.
CSCs↓, Salinomycin, a monocarboxylic polyether antibiotic isolated from Streptomyces albus, can precisely kill cancer stem cells (CSCs), particularly BCSCs, by various mechanisms, including apoptosis, autophagy, and necrosis.
Apoptosis↑,
TumAuto↑,
necrosis↑,
TumCP↓, salinomycin can inhibit cell proliferation, invasion, and migration in BC and reverse the immune-inhibitory microenvironment to prevent tumor growth and metastasis.
TumCI↓,
TumCMig↓,
TumCG↓,
TumMeta↓,
eff↑, Salinomycin is over 100 times more effective against BCSCs than paclitaxel, the traditional chemotherapy drug for the treatment of BC
Bcl-2↓, downregulation of Bcl-2 expression, and decreases their migration capacity, which is accompanied by downregulation of c-Myc and Snail expression
cMyc↓,
Snail↓,
ALDH↓, salinomycin reduces aldehyde dehydrogenase activity and the expression of MYC, AR, and ERG; it induces oxidative stress and inhibits nuclear factor (NF)-κB activity
Myc↓,
AR↓,
ROS↑, Salinomycin also induces autophagy by increasing intracellular ROS level, which is accompanied by MAPK signaling pathway activation
NF-kB↓,
PTCH1↓, significantly reduces tumor growth, which is accompanied by decreased PTCH, SMO, Gli1, and Gli2 expression
Smo↓,
Gli1↓,
GLI2↓,
Wnt↓, Figure 2
mTOR↓,
GSK‐3β↓,
cycD1/CCND1↓,
survivin↓,
P21↑,
p27↑,
CHOP↑,
Ca+2↑, cytosolic
DNAdam↑,
Hif1a↓,
VEGF↓,
angioG↓,
MMP↓, salinomycin can affect the cell membrane potential and reduce the level of ATP to induce mitophagy and mitoptosis.
ATP↓,
p‑P53↑, Salinomycin increases DNA breaks in BC cells as well as the expression of phosphorylated p53 and γH2AX in Hs578T cells.
γH2AX↑,
ChemoSen↑, Table 3 Synergistic anticancer co-action of salinomycin with other agents in BC.
ER Stress↑, SLM induces a potent endoplasmic reticulum (ER) stress followed by the trigger of the unfolded protein response (UPR) and an aberrant autophagic flux that culminated in necrosis due to mitochondria and lysosomal alterations.
UPR↑,
autoF↓, SLM treatment does not trigger apoptosis and blocks the autophagy flux in glioma cell line
lysosome↝,
ROS↑, aberrant autophagic flux was orchestrated by the production of Reactive Oxygen Species (ROS)
lipid-P↑, our data suggest that in our system the oxidative stress blocks the autophagic flux through lipid oxidation.
CSCs↓, SLM induces a potent antitumor effect in brain tumor stem cells (BTSCs) and established adult and pediatric glioma cell lines in vitro
necrosis↑, SLM induces necrosis cell death
ATP↓, with increasing doses of SLM displayed a decrease in intracellular ATP levels
MMP↓, SLM treated cells displayed significantly lower ΔΨm than untreated cells
MOMP↑, SLM induces mitochondrial MOMP.
DNAdam↑, We observed double strand breaks in SLM-treated cells (Figure 4C) and it is possible that this DNA damage is induced as a consequence of AIF internalization.
AIF↑,
lysoMP↑, hypothesis that SLM treatment triggers an autophagic process that cannot proceed adequately because of LMP resulting from oxidative stress.
MitoP↑, In addition, impairment of mitochondrial activity would trigger mitophagy, with engulfment of the organelle and initiation of autophagy.
Ca+2↑, The elevated levels of calcium and ROS inside mitochondria results in MOMP
Imm↑, A less recognized, albeit even more essential role of selenite is in its stimulation of the cellular immune system
angioG↑, certain studies indicate that selenite may inhibit angiogenesis, and help to repair the damaged DNA fragments.
DNArepair↑,
NK cell↑, most important function of this compound in the fighting of cancer may be the direct activation of natural killer (NK) cells.
ROS↑, thus selenite Se4+ exhibits an ability to undergo oxidation and reduction reactions (the so-called redox reactions)
AntiCan↑, It should be emphasized that the use of high doses of sodium selenite exhibits promising anticancer effects, as described in numerous preclinical studies
selectivity↑, Numerous studies demonstrated higher selenite cytotoxicity against cancer cells when compared to normal cells, using a comparable dose of this element
ER Stress↑, sodium selenite can cause cell death by an independent pathway of mitochondrial apoptosis, endoplasmic reticulum stress (caused by the presence of (non)unfolded proteins), processes of autophagy, or necrosis.
TumAuto↑,
necrosis↑,
toxicity↝, Sodium selenite may be toxic when taken orally at higher doses, yet it is well tolerated by other routes such as intravenous, intraperitoneal and/or transdermal
Dose↑, As demonstrated recently by Swedish scientists, considerably higher doses of selenium are well tolerated by patients with cancer, in the case when sodium selenite is administered intravenously.
TumCD↑, (1) selenite induced cancer cell death and apoptosis by producing superoxide radicals;
Apoptosis↑,
ROS↑,
eff↓, (2) selenite-induced superoxide production, cell death, and apoptosis were inhibited by overexpression of MnSOD, but not by CuZnSOD, CAT, or GPx1;
MMP↓, (3) selenite treatment resulted in a decrease in mitochondrial membrane potential, release of cytochrome c into the cytosol, and activation of caspases 9 and 3
Cyt‑c↑,
Casp3↑,
Casp9↑,
ER Stress↑, Studies have also shown that Se can induce cell death by mitochondrial-independent apoptotic pathways, endoplasmic reticulum stress, autophagy, or necrosis [11, 25, 43, 44]
TumAuto↑,
necrosis↑,
chemoPv↑, which may contribute to chemoprevention of prostate cancer.
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in-vitro, |
lymphoma, |
JPL119 |
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in-vitro, |
BC, |
MCF-7 |
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
BC, |
HS587T |
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in-vitro, |
Nor, |
NA |
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Apoptosis↑, ascorbic acid selectively killed cancer but not normal cells, using concentrations that could only be achieved by i.v. administration
necrosis↑,
H2O2↑,
*toxicity↓, pharmacologic concentrations of ascorbate killed cancer but not normal cells
All tested normal cells were insensitive to 20 mM ascorbate.
necrosis↑,
OS↑, long clinical remissions
H2O2↑,
DNAdam↑,
ROS↑,
Fenton↑,
Apoptosis↑, Moderate concentrations of H2O2 typically induce apoptosis
necrosis↑, higher H2O2 concentrations induce necrosis
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in-vitro, |
RCC, |
RCC4 |
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in-vitro, |
CRC, |
HCT116 |
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in-vitro, |
BC, |
MDA-MB-435 |
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in-vitro, |
Ovarian, |
SKOV3 |
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in-vitro, |
Colon, |
SW48 |
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in-vitro, |
GBM, |
U251 |
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eff↑, Here, we show that a Warburg effect triggered by activation of the hypoxia-inducible factor (HIF) pathway greatly enhances Vc-induced toxicity in multiple cancer cell lines
Warburg↓,
BioAv↑, HIF increases the intracellular uptake of oxidized Vc through its transcriptional target glucose transporter 1 (GLUT1),
ROS↑, resulting high levels of intracellular Vc induce oxidative stress and massive DNA damage, which then causes metabolic exhaustion by depleting cellular ATP reserves.
DNAdam↑,
ATP↓,
eff↑, Activation of HIF increases the susceptibility to Vc-induced cell toxicity
necrosis↑, High intracellular levels of Vc increase ROS and trigger necrosis in VHL-defective renal cancer cells.
PARP↑, Activation of the PARP Pathway by Vc Depletes Intracellular ATP Reserves in VHL-defective Renal Cancer Cells
Showing Research Papers: 1 to 27 of 27
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 27
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Fenton↑, 1, GSH↓, 2, H2O2↑, 2, lipid-P↑, 1, ROS↑, 13, mt-ROS↑, 1, Thiols↓, 1, TrxR↓, 1,
Metal & Cofactor Biology ⓘ
Zn2+↑, 1,
Mitochondria & Bioenergetics ⓘ
AIF↑, 1, ATP↓, 5, MMP↓, 6,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1, ENO1↓, 1, GlucoseCon↓, 1, Glycolysis↓, 1, HK2↓, 1, LDHA↓, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↓, 1, p‑Akt↓, 2, Apoptosis↑, 16, BAX↑, 1, Bcl-2↓, 3, Casp∅, 1, Casp3↑, 4, Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 1, Fas↑, 1, lysoMP↑, 1, MOMP↑, 1, Myc↓, 1, necrosis↑, 27, p27↑, 1, p38↓, 1, Pyro↑, 1, survivin↓, 1, TumCD↑, 3,
Transcription & Epigenetics ⓘ
other↑, 1, other↝, 1, tumCV↓, 2,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 3, HSP90↓, 1, UPR↑, 1,
Autophagy & Lysosomes ⓘ
autoF↓, 1, lysosome↝, 1, MitoP↑, 1, TumAuto↑, 5,
DNA Damage & Repair ⓘ
DNAdam↑, 6, DNArepair↑, 1, HR↓, 1, P53↑, 1, p‑P53↑, 2, PARP↑, 1, cl‑PARP↑, 4, RAD51↓, 1, γH2AX↑, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1, P21↑, 1, TumCCA↑, 6,
Proliferation, Differentiation & Cell State ⓘ
ALDH↓, 2, CSCs↓, 2, ERK↓, 1, ERK↑, 1, Gli1↓, 1, GSK‐3β↓, 1, IGF-1?, 1, mTOR↓, 3, p‑mTOR↓, 1, PI3K↓, 2, PTCH1↓, 1, PTEN↓, 1, PTEN↑, 1, Smo↓, 1, STAT3↑, 1, TumCG↓, 3, Wnt↓, 1, Zn2+↑, 1,
Migration ⓘ
Ca+2↑, 3, p‑FAK↓, 1, GLI2↓, 1, MMP9↓, 1, MUC4↓, 1, Snail↓, 1, TumCI↓, 2, TumCMig↓, 3, TumCP↓, 2, TumMeta↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, angioG↑, 1, HIF-1↓, 1, Hif1a↓, 2, VEGF↓, 3,
Barriers & Transport ⓘ
AQPs↓, 1, CellMemb↑, 2, GLUT1↓, 1, GLUT4↓, 1,
Immune & Inflammatory Signaling ⓘ
IFN-γ↓, 1, IL17↑, 1, IL2↑, 1, IL6↑, 1, Imm↑, 2, Inflam↓, 1, NF-kB↓, 3, NK cell↑, 1,
Cellular Microenvironment ⓘ
Temp∅, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 2, BioAv↝, 1, ChemoSen↑, 4, Dose↑, 1, Dose↝, 1, eff↓, 3, eff↑, 6, eff↝, 1, MRP1↓, 1, selectivity↑, 3,
Clinical Biomarkers ⓘ
AR↓, 1, IL6↑, 1, Myc↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 2, cardioP↑, 2, chemoPv↑, 1, hepatoP↑, 1, OS↑, 3, Remission↑, 1, toxicity↝, 2, TumVol↓, 2,
Total Targets: 131
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, GSH↑, 1, NRF2↑, 1, ROS↓, 1, uricA↓, 1,
Cell Death ⓘ
iNOS↓, 1,
Proliferation, Differentiation & Cell State ⓘ
STAT↓, 1, STAT3↓, 1,
Migration ⓘ
Cartilage↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL1↓, 1, IL6↓, 1, Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Protein Aggregation ⓘ
NLRP3↓, 1,
Drug Metabolism & Resistance ⓘ
Dose↝, 1, eff↑, 2, Half-Life↝, 1,
Clinical Biomarkers ⓘ
IL6↓, 1,
Functional Outcomes ⓘ
Pain↓, 1, toxicity↓, 1,
Total Targets: 22
Scientific Paper Hit Count for: necrosis, necrosis
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#:781 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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