tumCV Cancer Research Results

tumCV, Cell Viability: Click to Expand ⟱
Source:
Type:
Cell Viability
Scientific Papers found: Click to Expand⟱
4414- AgNPs,    Silver nanoparticles: Forging a new frontline in lung cancer therapy
- Review, Lung, NA
tumCV↑, AgNPs exhibit significant cytotoxic and apoptotic effects in lung cancer cell lines through mechanisms involving gene regulation, reactive oxygen species (ROS) production, and mitochondrial depolarization.
ROS↑,
MMP↓,
TumCCA↑, dose-dependent reductions in cell viability, cell cycle arrest, and apoptosis induction.
Apoptosis↑,
angioG↓, inhibit angiogenesis

5905- CAR,  HCQ,    Synergistic inhibition of metastatic melanoma by carvacrol and chloroquine: an in vitro and in silico investigation of apoptosis and molecular targets
- in-vitro, Melanoma, NA
eff↑, While carvacrol monotherapy exhibited weak cytotoxicity, its combination with non-toxic concentrations of chloroquine resulted in a potent and synergistic reduction in WM9 cell viability
tumCV↑,
IGF-1R↓, both carvacrol and chloroquine bind with high affinity to common molecular targets, including Insulin-Like Growth Factor 1 Receptor and Sirtuin-2.
SIRT2↓, CV and CQ may function as novel SIRT2 inhibitors
HSP90↓, Finally, our analysis confirmed that CQ, but not CV, strongly interacts with HSP90, a key chaperone protein that is frequently overexpressed in cancer
TumCP↓, Crucially, combining the two agents produced a powerful antiproliferative effect.
Akt↓, carvacrol has been shown to inhibit Akt activation in other cancer types [

4913- DSF,    Anticancer effects of disulfiram: a systematic review of in vitro, animal, and human studies
- Review, Var, NA
Apoptosis↑, Disulfiram (DSF), as an anti-alcoholic drug, kills the cancer cells by inducing apoptosis
tumCV↑, DSF was associated with enhanced apoptosis and tumor inhibition rates,
eff↑, The greatest anti-tumor activity was observed when DSF was used as combination therapy or as a nanoparticle-encapsulated molecule
toxicity↓, noticeable body weight loss after DSF treatment, which indicated that there was no major toxicity of DSF.
antiNeop↑, antineoplastic activity of DSF was first recorded in 1977
ChemoSen↑, The synergistic effect of Cis, DOX, TMZ, PTX, Gy, and DSF in induced apoptosis was significantly higher than that of DSF or Cis or DOX or TMZ or Gy alone
RadioS↑, Tumor cell growth was significantly inhibited when DSF, chemotherapy, and radiation therapy were used simultaneously, as shown in the examined in vivo studies
OS↑, All three studies show that DSF is safe and seems to prolong survival of cancer patients
ROS↑, Metabolites of DSF chelate with metal ions, leading to alterations in the intracellular levels of metal ions, enhancement of oxidative stress, inhibition of the activities of superoxide dismutase or matrix metalloproteinases,
SOD↓,
MMP1↓,
eff↑, observation that the combination of DSF with metal ions (Cu, Ag) leads to enhanced anticancer effectiveness is in accordance with the observations of in vitro and animal experiments
Half-Life↓, At the pH of 7.4, the half-life of DSF is 1–1.5 min

975- Est,    Estrogen inhibits autophagy and promotes growth of endometrial cancer by promoting glutamine metabolism
- vitro+vivo, UEC, NA
GLS↑, in estrogen-sensitive UEC cell (UECC) (an ER inhibitor antagonist) could reverse these effects.
cMyc↑, three MYC subtypes (c-MYC, n-MYC and l-MYC) were increased after estrogen treatment
GlutMet↑,
tumCV↑,
TumAuto↓,

4509- GLA,    Gamma-linolenic Acid (GLA) sensitizes pancreatic cancer cells to gemcitabine
- in-vitro, PC, PANC1
tumCV↑, The nutritional supplement gamma-linolenic acid (GLA) is a poly-unsaturated fatty acid (PUFA) of the n-6 PUFA family, and has garnered attention for its cytotoxic effects against tumor cell lines while not affecting normal cells.
selectivity↑,
ChemoSen↑, When GLA is combined with GEM, the results are synergistically enhanced

2249- MF,    Pulsed electromagnetic fields modulate energy metabolism during wound healing process: an in vitro model study
- in-vitro, Nor, L929
*TumCMig↑, PEMFs with specific parameter (4mT, 80 Hz) promoted cell migration and viability.
*tumCV↑,
*Glycolysis↑, PEMFs-exposed L929 cells was highly glycolytic for energy generation
*ROS↓, PEMFs enhanced intracellular acidification and maintained low level of intracellular ROS in L929 cells.
*mitResp↓, shifting from mitochondrial respiration to glycolysis
*other↝, Furthermore, the analysis of ECAR/ OCR basal ratio demonstrated a tendency toward to glycolytic phenotype in L929 cells under PEMF exposure, compared to control group
*OXPHOS↓, PEMFs promoted the transformation of energy metabolism pattern from oxidative phosphorylation to aerobic glycolysis
*pH↑, result of pH detection by flow cytometer indicated the pH level in L929 cells was significantly increased in the PEMFs group compared to the control group
*antiOx↑, PEMFs upregulated the expression of antioxidant or glycolysis related genes
*PFKM↑, Pfkm, Pfkl, Pfkp, Pkm2, Hk2, Glut1, were also significantly up-regulated in the PEMFs group
*PFKL↑,
*PKM2↑,
*HK2↑,
*GLUT1↑,
*GPx1↑, GPX1, GPX4 and Sod 1 expression were significantly higher in the PEMFs group compared to the control group
*GPx4↑,
*SOD1↑,

2005- PLB,    Plumbagin induces apoptosis in lymphoma cells via oxidative stress mediated glutathionylation and inhibition of mitogen-activated protein kinase phosphatases (MKP1/2)
- in-vivo, Nor, EL4 - in-vitro, AML, Jurkat
JNK↑, Plumbagin induced persistent activation of JNK
Cyt‑c↑, plumbagin induced cytochrome c release, FasL expression and Bax levels via activation of JNK pathway
FasL↑,
BAX↑,
ROS↑, plumbagin has been reported to induce ROS in normal as well as in tumor cells
*ROS↑, induce ROS in normal as well as in tumor cells
MKP1↓, plumbagin induced oxidative stress may suppress MKP activity in lymphoma cells leading to sustained JNK activation resulting in apoptosis.
MKP2↓,
selectivity∅, Plumbagin induced cell death in EL4(normal) cells and Jurkat cells
tumCV↑, cell viability dramatically decreased with increasing concentrations of plumbagin (0.05-2.5uM) when incubated for 24 or 48 h
Cyt‑c↑, Bax dependent cytochrome c release and apoptosome complex formation is followed by the cleavage of pro-caspase-3
Casp3↑,
GSH/GSSG↓, progressive decrease in GSH/GSSG ratio in tumor cells following plumbagin treatment
ROS↑, simultaneous increase in the levels of intracellular ROS was observed in both these cell lines which remained high up to 4 h indicating an increase in oxidative stress in tumor cells
mt-ROS↑, While we observed low basal mtROS levels in untreated cells, plumbagin treatment resulted in a significant increase in mtROS levels
*ROS↑, both cell lines, meaning normal EL4 cells too
eff↓, NAC, GSH and PEG-catalase were able to abrogate plumbagin induced ROS and cell death.

1132- RT,    Rutin Promotes Proliferation and Orchestrates Epithelial–Mesenchymal Transition and Angiogenesis in MCF-7 and MDA-MB-231 Breast Cancer Cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
Vim↑,
N-cadherin↑, CDH2
E-cadherin↓,
TumCP↑,
TumCMig↑,
tumCV↑, increased the number of viable cells at concentrations more than 200 µM.
MKI67↑, rutin (200 μM)

2107- TQ,    Cytotoxicity of Nigella sativa seed oil and extract against human lung cancer cell line
- in-vitro, Lung, A549
tumCV↑, NSE and NSO significantly reduce the cell viability and alter the cellular morphology of A-549 cells in a concentration dependent manner


Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH/GSSG↓, 1,   ROS↑, 4,   mt-ROS↑, 1,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↑, 1,   GLS↑, 1,   GlutMet↑, 1,   SIRT2↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Casp3↑, 1,   Cyt‑c↑, 2,   FasL↑, 1,   JNK↑, 1,   MKP1↓, 1,   MKP2↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↑, 8,  

Protein Folding & ER Stress ⓘ

HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1R↓, 1,  

Migration ⓘ

E-cadherin↓, 1,   MMP1↓, 1,   N-cadherin↑, 1,   TumCMig↑, 1,   TumCP↓, 1,   TumCP↑, 1,   Vim↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   eff↓, 1,   eff↑, 3,   Half-Life↓, 1,   RadioS↑, 1,   selectivity↑, 1,   selectivity∅, 1,  

Functional Outcomes ⓘ

antiNeop↑, 1,   MKI67↑, 1,   OS↑, 1,   toxicity↓, 1,  
Total Targets: 42

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GPx1↑, 1,   GPx4↑, 1,   OXPHOS↓, 1,   ROS↓, 1,   ROS↑, 2,   SOD1↑, 1,  

Mitochondria & Bioenergetics ⓘ

mitResp↓, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↑, 1,   HK2↑, 1,   PFKL↑, 1,   PFKM↑, 1,   PKM2↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,   tumCV↑, 1,  

Migration ⓘ

TumCMig↑, 1,  

Barriers & Transport ⓘ

GLUT1↑, 1,  

Cellular Microenvironment ⓘ

pH↑, 1,  
Total Targets: 18

Scientific Paper Hit Count for: tumCV, Cell Viability
1 Silver-NanoParticles
1 Carvacrol
1 hydroxychloroquine
1 Disulfiram
1 Estrogen
1 γ-linolenic acid (Borage Oil)
1 Magnetic Fields
1 Plumbagin
1 Rutin
1 Thymoquinone
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

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