CAIX Cancer Research Results
CAIX, Carbonic Anhydrase IX: Click to Expand ⟱
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CAIX (Carbonic Anhydrase IX) is a transmembrane enzyme that plays a crucial role in maintaining the pH balance in cells and their surroundings. In the context of cancer, CAIX has been found to be overexpressed in various types of tumors.
CAIX is overexpressed in cancer cells compared to normal cells. This overexpression is thought to contribute to the increased ability of cancer cells to survive and grow in hypoxic environments.
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Scientific Papers found: Click to Expand⟱
AntiCan↑, FA has anti-inflammatory, analgesic, anti-radiation, and immune-enhancing effects and also shows anticancer activity,
Inflam↓,
RadioS↑,
ROS↑, FA can cause mitochondrial apoptosis by inducing the generation of intracellular reactive oxygen species (ROS)
Apoptosis↑,
TumCCA↑, G0/G1 phase
TumCMig↑, inducing autophagy; inhibiting cell migration, invasion, and angiogenesis
TumCI↓,
angioG↓,
ChemoSen↑, synergistically improving the efficacy of chemotherapy drugs and reducing adverse reactions.
ChemoSideEff↓,
P53↑, FA could increase the expression level of p53 in MIA PaCa-2 pancreatic cancer cells
cycD1/CCND1↓, while reducing the expression levels of cyclin D1 and cyclin-dependent kinase (CDK) 4/6.
CDK4↓,
CDK6↓,
TumW↓, FA treatment was found to reduce tumor weight in a dose-dependent manner, increase miR-34a expression, downregulate Bcl-2 protein expression, and upregulate caspase-3 protein expression
miR-34a↑,
Bcl-2↓,
Casp3↑,
BAX↑,
β-catenin/ZEB1↓, isoferulic acid dose-dependently downregulated the expression of β-catenin and MYC proto-oncogene (c-Myc), inducing apoptosis
cMyc↓,
Bax:Bcl2↑, FXS-3 can inhibit the activity of A549 cells by upregulating the Bax/Bcl-2 ratio
SOD↓, After treatment with FA, Cao et al. [40] observed an increase in ROS production and a decrease in superoxide dismutase activity and glutathione content in EC-1 and TE-4 oesophageal cancer cells
GSH↓,
LDH↓, FA could promote the release of lactate dehydrogenase (LDH)
ERK↑, A can activate the ERK1/2 pathway
eff↑, conjugated zinc oxide nanoparticles with FA (ZnONPs-FA) to act on hepatoma Huh-7 and HepG2 cells. The results showed that ZnONPs-FA could induce oxidative DNA damage and apoptosis by inducing ROS production.
JAK2↓, by inhibiting the JAK2/STAT6 immune signaling pathway
STAT6↓,
NF-kB↓, thus inhibiting the activation of NF-κB
PYCR1↓, FA can target PYCR1 and inhibit its enzyme activity in a concentration-dependent manner.
PI3K↓, FA inhibits the activation of the PI3K/AKT pathway
Akt↓,
mTOR↓, FA could significantly reduce the expression level of mTOR mRNA and Ki-67 protein in A549 lung cancer graft tissue
Ki-67↓,
VEGF↓,
FGFR1↓, FA is a novel FGFR1 inhibitor
EMT↓, FA can inhibit EMT
CAIX↓, selectively inhibit CAIX
LC3II↑, Autophagy vacuoles and increased LC3-II and p62 autophagy proteins were observed after treatment with this compound
p62↑,
PKM2↓, FA could inhibit the expression of PKM2 and block aerobic glycolysis
Glycolysis↓,
*BioAv↓, FA has poor solubility in water and a poor ability to pass through biological barriers [118]; therefore, the extent to which it is metabolized in vivo after oral administration is largely unknown
Apoptosis↑,
Bcl-2↓,
P53↑, up-regulated expression of p53,
cl‑Casp3↑,
Cyt‑c↑,
ROS↑, induced ROS production by suppressing the expression of antioxidant regulatory enzymes, namely superoxide dismutase and catalase
SOD↓,
Catalase↓,
Glycolysis↓,
GLUT3↓,
LDHA↓, LDHA inhibitor
MCT1↓,
NHE1↓,
ATPase↓,
CAIX↓,
NRF2↑, chemopreventive properties that are thought to be due to potent upregulation of Nrf2
ChemoSideEff↓, chemopreventive properties
eff↑, combined SFN with taxol in treatment of prostate cancer cell line DU145, and observed that SFN potentiated the effects of low doses of taxol
TumCP↓,
Apoptosis↑,
TumCCA↑, induce G2/M cell cycle arrest in vitro and in vivo
eff↑, SFN positively enhanced bortezomib, lenalidomide, and conventional drugs, such as dexamethasone, doxorubicin, and melphalan in a synergistic manner
PSA↓, SFN has shown to significantly reduce levels of prostate-specific antigen (PSA) (44.4% SFN group vs. 71.8% in placebo)
P53↑, SFN activates various anti-cancer responses such as p53, ARE, IRF-1, Pax-6 and XRE while suppressing proteins involved in tumorigenesis and progression, such as HIF1α, AP-1 and CA IX
Hif1a↓, while suppressing proteins involved in tumorigenesis and progression, such as HIF1α, AP-1 and CA IX
CAIX↓,
chemoR↓, SFN has thus shown to reduce chemoresistance and may be a potential agent to be used in conjunction with chemotherapeutics
5HT↓, SFN downregulates 5-HT receptor expression in Caco-2 cells
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in-vitro, |
RCC, |
RCC4 |
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in-vitro, |
RCC, |
Caki-1 |
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Hif1a↓, TQ reduced HIF-1α protein levels in renal cancer cells. In addition, decreased HIF-1α levels in both cytoplasm and nucleus after treatment with 10 μM of TQ were observed in Caki-1 cells
eff↝, suggesting that suppression of HIF-1α by TQ may be connected to Hsp90-mediated HIF-1α stabilization
uPAR↓, significantly downregulated the hypoxia-induced tumor promoting HIF-1α target genes, such as FN1, LOXL2, uPAR, VEGF, CA-IX, PDK1, GLUT1, and LDHA, in TQ-treated Caki-1
VEGF↓,
CAIX↓,
PDK1↓,
GLUT1↓,
LDHA↓,
Glycolysis↓, we found that TQ significantly increases glucose levels in hypoxic Caki-1 and A498 cultured medium, indicating that hypoxia-induced anaerobic glycolysis is significantly suppressed by TQ treatment
e-lactateProd↓, Consistent with suppression of hypoxic glycolysis by TQ treatment, increased extracellular lactate levels under hypoxia were decreased in TQ-treated Caki-1 and A498 renal cancer cells
i-ATP↓, intracellular ATP levels were significantly decreased in TQ-treated Caki-1 and A498 cells under hypoxia
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 ⓘ
Catalase↓, 1, GSH↓, 1, NRF2↑, 1, PYCR1↓, 1, ROS↑, 2, SOD↓, 2,
Mitochondria & Bioenergetics ⓘ
i-ATP↓, 1, FGFR1↓, 1,
Core Metabolism/Glycolysis ⓘ
CAIX↓, 4, cMyc↓, 1, Glycolysis↓, 3, e-lactateProd↓, 1, LDH↓, 1, LDHA↓, 2, PDK1↓, 1, PKM2↓, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↑, 3, BAX↑, 1, Bax:Bcl2↑, 1, Bcl-2↓, 2, Casp3↑, 1, cl‑Casp3↑, 1, Cyt‑c↑, 1, MCT1↓, 1,
Autophagy & Lysosomes ⓘ
LC3II↑, 1, p62↑, 1,
DNA Damage & Repair ⓘ
P53↑, 3,
Cell Cycle & Senescence ⓘ
CDK4↓, 1, cycD1/CCND1↓, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, ERK↑, 1, miR-34a↑, 1, mTOR↓, 1, PI3K↓, 1, STAT6↓, 1,
Migration ⓘ
ATPase↓, 1, Ki-67↓, 1, TumCI↓, 1, TumCMig↑, 1, TumCP↓, 1, uPAR↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, Hif1a↓, 2, VEGF↓, 2,
Barriers & Transport ⓘ
GLUT1↓, 1, GLUT3↓, 1, NHE1↓, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1, JAK2↓, 1, NF-kB↓, 1, PSA↓, 1,
Synaptic & Neurotransmission ⓘ
5HT↓, 1,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 1,
Drug Metabolism & Resistance ⓘ
chemoR↓, 1, ChemoSen↑, 1, eff↑, 3, eff↝, 1, RadioS↑, 1,
Clinical Biomarkers ⓘ
Ki-67↓, 1, LDH↓, 1, PSA↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, ChemoSideEff↓, 2, TumW↓, 1,
Total Targets: 67
Pathway results for Effect on Normal Cells:
Drug Metabolism & Resistance ⓘ
BioAv↓, 1,
Total Targets: 1
Scientific Paper Hit Count for: CAIX, Carbonic Anhydrase IX
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#:929 State#:% Dir#:1
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