CXCR2 Cancer Research Results
CXCR2, CXCR2: Click to Expand ⟱
| Source: |
| Type: chemokine receptor |
CXCR2 is a chemokine receptor that plays a crucial role in the progression and metastasis of various types of cancer.
CXCR2 is often over expression and is associated with poor prognosis and increased risk of metastasis.
Several CXCR2 inhibitors, such as SB225002 and AZD5069, have been developed and are being evaluated in preclinical and clinical studies for their potential to treat various types of cancer.
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Scientific Papers found: Click to Expand⟱
Apoptosis↑, anticancer activity of nimbolide related to induction of apoptosis and cell cycle arrest; and inhibition of signaling pathways related to cancer progression.
TumCCA↑,
TumCP↓, oxidative DNA damage, upregulation of antioxidant and induction of apoptosis, inhibition of tumor cell proliferation, invasion, angiogenesis, and metastasis
TumCI↓,
angioG↓,
TumMeta↓,
PTEN↑, significant increase in the protein expression of PTEN upon nimbolide treatment in breast cancer cell lines
NF-kB↓, nimbolide exerts potent anticancer effects in HepG2 cells by inhibiting NF-κB activation and its downstream events, such as activation of the Wnt/β-catenin
Wnt↓,
β-catenin/ZEB1↓,
IKKα↓, Nimbolide significantly decreased the protein expression of IKKα, IKKβ, and NF-κB in breast cancer cell lines
CXCR2↓, CCR2, CXCR1, CXCR2, and CXCR4 is significantly decreased in nimbolide-treated breast cancer cell lines
CXCR4↓,
Bcl-2↓, imbolide has been shown to interfere with the expression of NF-κB-regulated proteins, like Bcl-2, cyclooxygenase 2, MMP-9, and VEGF, by inhibiting IKK.
COX2↓,
MMP9↓,
VEGF↓,
TIMP2↑, TIMP-2 expression is increased in nimbolide-treated breast cancer cells
chemoPv↑, nimbolide (100 µg/kg) has been shown to exhibit chemopreventive activity against 7,12-dimethylbenzanthracene (DMBA) 3
ROS↑, Nimbolide sensitizes human colon cancer cell lines (HCT-116 and HT-29) to TRAIL through reactive oxygen species-
DR4↑, and Erk-dependent up-regulation of death receptors, p53, and Bax.
P53↑,
BAX↑,
Casp3↑, nimbolide activates caspase-3, -8, and -9, which favors the cleavage of poly(ADP) ribose polymerase into 115- and 85-kDa peptides, thus inducing apoptosis in breast cancer cell lines
Casp8↑,
Casp9↑,
cl‑PARP↑,
Mcl-1↓, figure 4
XIAP↓,
survivin↓,
FasL↑,
FADD↑,
EGFR↓,
MMPs↓,
TumCP↓, anti-proliferation, induction of apoptosis, inhibition of metastasis and angiogenesis, and modulation of carcinogen-metabolizing enzymes.
Apoptosis↓,
TumMeta↑,
angioG↓,
*antiOx↑, nimbolidehas been found to possess antioxidant effect and free radical scavenging activities.
*eff↑, In comparison to azadirachtin and ascorbic acid (vitamin C), nimbolide was shown to be a more potent antioxidant
Apoptosis↑, Nimbolide induces apoptosis through diverse molecular mechanism(s).
MOMP↑, Nimbolide disrupts MOMP, which promotes caspases activation leading to apoptosis.
CDK1↓, Nimbolide also reduces the level of CDKs and cyclins, causing cell cycle arrest.
TumCCA↑,
MAPK↓, Nimbolide also abrogates various signaling cascades including MAPK (ERK1/2), JAK2/STAT3 and PI3K/Akt, leading to suppression of proliferation of a wide variety of human cancer cells.
JAK2↓,
STAT3↓,
PI3K↓,
Akt↓,
TumCP↓,
*NRF2↑, Nimbolide disrupts the Nrf2-KEAP1 complex and promotes the release of Nrf2, thus increasing levels of antioxidant and detoxification enzymes.
NF-kB↓, Inhibition of the NF-κB pathway also reduces the dissociation of GSK-3β from β-catenin, hence restraining the Wnt/β-catenin
GSK‐3β↑,
Wnt↓,
β-catenin/ZEB1↓,
chemoPv↑, nimbolide showed remarkable chemopreventive property.
Bcl-xL↓, Nimbolide treatmentdecreased the expression of antiapoptotic proteins(Bcl-xL, Bcl-2, survivin, caspase inhibitor molecules) and increased the expression of proapoptotic proteins (cytochrome c, Bax, Bad, Bid, cleaved caspases) in prostate cancer cells
Bcl-2↓,
survivin↓,
Cyt‑c↑,
BAX↑,
BID↑,
cl‑Casp↑,
P53↑, nimbolide acted by up-regulation of p53 levelin HeLa cells, thereby priming these cells towards apoptosis by destabilizing the mitochondria
DR5↑, Nimbolide up-regulated the expression of both DR5 and DR4 in chronic myeloid leukemia (KBM-5), multiple myeloma (U266), embryonic kidney carcinoma (A293), pancreatic adenocarcinoma (AsPC-1), and breast adenocarcinoma (MDA-MB-231) cells
DR4↑,
ROS↑, nimbolide resulted in generation of reactive oxygen species (ROS)
lipid-P↑, ROS also induced lipid peroxidation of cellular membranes, generating toxic metabolites such as malondialdehyde (MDA) that can react with DNA to form adducts to induce apoptosis.
MDA↑,
MMP2↓, nimbolide reduced mRNA expression of MMP-2, MMP-9, uPA and uPA receptor in breast cancer cells (MCF-7)
MMP9↓,
uPA↓,
ICAM-1↓, nimbolide was shown to downregulate the expression of MMP-9, ICAM-1, and CXCR4 in colorectal cancer xenografts
CXCR4↓,
CXCR2↓, nimbolide also reduced expression of CXCL8 and CXCR2 in breast cancers, and thus abrogated angiogenesis
angioG↓,
BBB↑, nimbolide might be able to cross blood-brain barrier (BBB) and the concentration could be sufficient for nimbolide to suppress intracranial tumour cell proliferation.
Showing Research Papers: 1 to 2 of 2
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
lipid-P↑, 1, MDA↑, 1, ROS↑, 2,
Mitochondria & Bioenergetics(tgid=3) ⓘ
XIAP↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↓, 1, Apoptosis↑, 2, BAX↑, 2, Bcl-2↓, 2, Bcl-xL↓, 1, BID↑, 1, cl‑Casp↑, 1, Casp3↑, 1, Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 1, DR4↑, 2, DR5↑, 1, FADD↑, 1, FasL↑, 1, MAPK↓, 1, Mcl-1↓, 1, MOMP↑, 1, survivin↓, 2,
DNA Damage & Repair(tgid=10) ⓘ
P53↑, 2, cl‑PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
GSK‐3β↑, 1, PI3K↓, 1, PTEN↑, 1, STAT3↓, 1, Wnt↓, 2,
Migration(tgid=13) ⓘ
MMP2↓, 1, MMP9↓, 2, MMPs↓, 1, TIMP2↑, 1, TumCI↓, 1, TumCP↓, 3, TumMeta↓, 1, TumMeta↑, 1, uPA↓, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 3, EGFR↓, 1, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 1, CXCR2↓, 2, CXCR4↓, 2, ICAM-1↓, 1, IKKα↓, 1, JAK2↓, 1, NF-kB↓, 2,
Clinical Biomarkers(tgid=22) ⓘ
EGFR↓, 1,
Functional Outcomes(tgid=23) ⓘ
chemoPv↑, 2,
Total Targets: 56
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, NRF2↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
eff↑, 1,
Total Targets: 3
Scientific Paper Hit Count for: CXCR2, CXCR2
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#:921 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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