tumCV Cancer Research Results
tumCV, Cell Viability: Click to Expand ⟱
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Cell Viability
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Scientific Papers found: Click to Expand⟱
ROS↓, Pretreatment with N-acetyl cysteine (ROS scavenger) or 4-phenylbutyric acid (4-PBA; ER stress inhibitor) significantly alleviated apoptosis, mitochondrial ROS production, mitochondrial dysfunction and ER stress response in a dose-dependent manner.
tumCV∅, There was no difference in cell viability between the SiHa cells treated with 2 mM 4-PBA for 6 h and cell in the untreated control group
cl‑PARP↓, Surprisingly, 4-PBA pretreatment attenuated the levels of cleaved PARP and caspase-3 in T. vaginalis-infected SiHa cells in a dose-dependent manner
cl‑Casp3↓,
MMP∅, T. vaginalis induced MMP depolarization in the SiHa cells; however, these changes in fluorescence were suppressed by 4-PBA pretreatment
ER Stress↓, pretreatment with the ER stress inhibitor 4-PBA was found to significantly attenuate the levels of ER stress-related proteins in T. vaginalis-infected cells
TumCD∅, We found that PSO and RA-RF were not toxic to TNF-α-induced A549 cells.
ROS↓, Both extracts significantly decreased the generation of reactive oxygen species (ROS) in this cell line.
IL1β↓, mRNA expression levels of IL-1β, IL-6, IL-8, TNF-α, and COX-2 were significantly decreased by the treatment of PSO and RA-RF.
IL6↓,
IL8↓,
TNF-α↓,
COX2↓,
SOD2↓, MnSOD, FOXO1, and NF-κB and phosphorylation of JNK were also significantly diminished by PSO and RA-RF treatment
FOXO1↓,
NF-kB↓,
JNK↓,
antiOx↑, PSO and RA-RF act as antioxidants
tumCV∅, PSO and RA-RF had no effect on A549 cell viability.
*HO-1↑, TQ induced the expression of HO-1 in HaCaT/ Cells treated with TQ (1, 5, 10, 20 lM) for 6 h induced the expression of HO-1 protein. maximal induction observed until 12 h and then returned to basal level time thereafter
*NRF2↑, Treatment with TQ increased the localization of nuclear factor (NF)-erythroid2-(E2)-related factor-2 (Nrf2) in the nucleus and elevated the antioxidant response element (ARE)-reporter gene activity.
*e-ERK↑, TQ induced the phosphorylation of extracellular signal-regulated kinase (ERK), Akt and cyclic AMP-activated protein kinase-α (AMPKα).
*e-Akt↑,
*AMPKα↑,
*ROS⇅, Treatment of HaCaT cells with TQ resulted in a concentration-dependent increase in the intracellular accumulation of ROS (most occurs at 20uM concentration -see figure 5A) (later it drops the ROS)
*eff↓, pretreatment with N-acetyl cysteine (NAC) abrogated TQ-induced ROS accumulation, Akt and AMPKα activation, Nrf2 nuclear localization, the ARE-luciferase activity, and HO-1 expression in HaCaT cells
*tumCV∅, does not change much 1-20uM of TQ (normal cells) see figure 1A
Dose∅, However, intense exercise is physically challenging for bedridden, disabled, or aged patients. As an exercise surrogate, low-magnitude (<1 g) high-frequency (>30 Hz) (LMHF) vibration has gained growing interest
TumMeta↑, These data indicated that LMHF vibration could inhibit cancer extravasation, suggesting that vibration may suppress bone metastasis in breast cancer patients.
eff∅, Nevertheless, recent clinical studies indicated that LMHF vibration had minimum or no beneficial effects for the elderly (>65 years old)
Piezo1↑, LMHF vibration (60 Hz, 0.3 g, 1 h, Figure 1) significantly up-regulated the expressions of Piezo1 (1.63-fold) and COX-2 (1.32-fold) and down-regulated the expression of RANKL (0.86-fold).
COX2↑,
RANKL↓, down-regulated the expression of RANKL (0.86-fold).
TumCG∅, Vibration (60 Hz, 0.3 g, 1 h/day for 3 days) did not significantly impact cell growth and viability
tumCV∅,
TumCI↓, Vibration reduced breast cancer invasion via direct and indirect osteocyte signaling. vibration decreased cancer invasion distance by 24%
Showing Research Papers: 1 to 4 of 4
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, ROS↓, 2, SOD2↓, 1,
Mitochondria & Bioenergetics ⓘ
MMP∅, 1,
Cell Death ⓘ
cl‑Casp3↓, 1, JNK↓, 1, TumCD∅, 1,
Transcription & Epigenetics ⓘ
tumCV∅, 3,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1,
DNA Damage & Repair ⓘ
cl‑PARP↓, 1,
Proliferation, Differentiation & Cell State ⓘ
FOXO1↓, 1, Piezo1↑, 1, TumCG∅, 1,
Migration ⓘ
TumCI↓, 1, TumMeta↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, COX2↑, 1, IL1β↓, 1, IL6↓, 1, IL8↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Hormonal & Nuclear Receptors ⓘ
RANKL↓, 1,
Drug Metabolism & Resistance ⓘ
Dose∅, 1, eff∅, 1,
Clinical Biomarkers ⓘ
IL6↓, 1,
Total Targets: 26
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
HO-1↑, 1, NRF2↑, 1, ROS⇅, 1,
Cell Death ⓘ
e-Akt↑, 1,
Kinase & Signal Transduction ⓘ
AMPKα↑, 1,
Transcription & Epigenetics ⓘ
tumCV∅, 1,
Proliferation, Differentiation & Cell State ⓘ
e-ERK↑, 1,
Drug Metabolism & Resistance ⓘ
eff↓, 1,
Total Targets: 8
Scientific Paper Hit Count for: tumCV, Cell Viability
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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