Hypoxia Cancer Research Results
Hypoxia, Hypoxia: Click to Expand ⟱
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Deprived of adequate oxygen supply at the tissue level.
Hypoxia, a condition characterized by insufficient oxygen levels in tissues.
Cancer cells can adapt to hypoxic conditions through various mechanisms. They may activate hypoxia-inducible factors (HIFs), which are transcription factors that help cells respond to low oxygen levels. HIFs promote the expression of genes involved in angiogenesis (formation of new blood vessels), metabolism, and survival.
Tumors with high levels of hypoxia may be more aggressive and less responsive to treatment.
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Scientific Papers found: Click to Expand⟱
TumCP↓, β-caryophyllene (BCP) exhibits anti-proliferative properties in cancer cells.
CB2 / CNR2↓, BCP is able to interact with the CB2 receptor with nM affinity although the concentrations that affect signaling are in the low μM range
STAT3↓, BCP also reduces proliferation by blocking the STAT3/mTOR/AKT signaling path
mTOR↓,
Akt↓,
Hypoxia↓, we hypothesized that BCP might reverse the hypoxic phenotype of TNBC cells.
other↝, Cancer cells exhibit a unique metabolic preference for the glycolytic pathway over oxidative phosphorylation for maintaining the tumor microenvironment.
Glycolysis↓, Diclofenac (DCF), a nonsteroidal anti-inflammatory drug, has been shown to exhibit anticancer effects by interfering with the glucose metabolism pathway.
LDHA↓, DCF binds to LDHA adjacent to the substrate binding site and inhibits its activity in a dose-dependent and allosteric manner in HeLa cells.
Hypoxia↓, Thus, DCF inhibits the hypoxic microenvironment and induces apoptosis-mediated cell death.
Apoptosis↑,
lactateProd↓, DCF-induced LDHA inhibition alters pyruvate, lactate, NAD+, and ATP production in cells, and this could be a possible mechanism through which DCF inhibits glucose uptake in cancer cells.
ATP↓, DCF-induced ATP deprivation leads to mitochondria-mediated oxidative stress, which results in DNA damage, lipid peroxidation, and apoptosis-mediated cell death.
mt-ROS↑,
DNAdam↑,
lipid-P↑,
AMPK↑, Reduction in intracellular ATP levels additionally activates the sensor kinase, adenosine monophosphate-activated protein kinase (AMPK), which further downregulates phosphorylated ribosomal S6 kinase (p-S6K), leading to apoptosis-mediated cell death.
p‑S6K↓,
TumCP↓, DCF inhibits proliferation in HeLa cells
Dose↝, HeLa cells with an IC50 dose of 175 ± 4.86 μm on 24 h of incubation
selectivity↑, DCF did not significantly affect the viability of normal cervical cells at 175 μm (IC50 dose in HeLa cells), where the IC50 value was found to be greater than 1 mm concentration of DCF (
i-MDA↑, The result showed that DCF treatment in HeLa cells led to a significant increase in MDA levels, suggesting an increased level of lipid peroxidation
mtDam↑, Many reports suggest that there is a strong correlation between the inhibition of LDHA and the induction of oxidative stress (ROS production) via mitochondrial damage
*Hypoxia↓, Neurotrophin-3, originating from Müller glial cells in the retina, plays a key role in protecting photoreceptors from damage induced by light or hypoxia.
*NTF3/NT-3↑, we demonstrated that the water extract of E. longifolia roots enhanced neurotrophin-3 gene expression in primary rat Müller cells.
*other↑, this study suggests that E. longifolia may be promising for improving eye health and must be further investigated.
*Half-Life↓, However, their clinical application presents challenges owing to their short plasma half-life (1.28 and 0.92 min for NT3 and BDNF, respectively) after intravenous administration
Hypoxia↓,
mitResp↓,
ROS↑, the production of reactive oxygen species would be increase which, in turn, improves the efficacy of PDT against hypoxic tumors.
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(tgid=1) ⓘ
lipid-P↑, 1, i-MDA↑, 1, ROS↑, 1, mt-ROS↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, mitResp↓, 1, mtDam↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, Glycolysis↓, 1, lactateProd↓, 1, LDHA↓, 1, p‑S6K↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↝, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
mTOR↓, 1, STAT3↓, 1,
Migration(tgid=13) ⓘ
TumCP↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
Hypoxia↓, 3,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CB2 / CNR2↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
Dose↝, 1, selectivity↑, 1,
Total Targets: 23
Pathway results for Effect on Normal Cells:
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
Hypoxia↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
NTF3/NT-3↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
Half-Life↓, 1,
Total Targets: 4
Scientific Paper Hit Count for: Hypoxia, Hypoxia
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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