MIP2 Cancer Research Results

MIP2, Macrophage Inflammatory Protein 2: Click to Expand ⟱
Source:
Type: chemokine
Macrophage Inflammatory Protein 2 (MIP-2) is a chemokine that plays a role in the recruitment of immune cells to sites of inflammation.
MIP-2 is produced by various cell types, including macrophages, epithelial cells, and cancer cells themselves. It acts by binding to its receptors, CXCR1 and CXCR2, which are expressed on the surface of immune cells, such as neutrophils and macrophages.
Scientific Papers found: Click to Expand⟱
3667- ART/DHA,    Artemisinin improves neurocognitive deficits associated with sepsis by activating the AMPK axis in microglia
- Review, Sepsis, NA
*cognitive↑, artemisinin administration significantly improved LPS-induced cognitive impairments assessed in Morris water maze and Y maze tests
*neuroP↑, attenuated neuronal damage and microglial activation in the hippocampus.
*TNF-α↓, artemisinin (40 μΜ) significantly reduced the production of proinflammatory cytokines (i.e., TNF-α, IL-6)
*IL6↓,
*NF-kB↓, artemisinin significantly suppressed the nuclear translocation of NF-κB and the expression of proinflammatory cytokines by activating the AMPKα1 pathway;
*AMPK↑,
*ROS↓, artemisinin protects neuronal HT-22 cells from oxidative injury by activating the Akt pathway
*Akt↑,
*MCP1/CCL2↓, artemisinin reversed the LPS-induced increases in the chemokines MCP-1 and MIP-2
*MIP2↓,
*TGF-β↑, Artemisinin also significantly increased the mRNA and protein expression of TGF-β
*Inflam↓, The AMPKα1 pathway is involved in the anti-inflammatory effect of artemisinin

556- ART/DHA,    Artemisinins as a novel anti-cancer therapy: Targeting a global cancer pandemic through drug repurposing
- Review, NA, NA
IL6↓,
IL1↓, IL-1β
TNF-α↓,
TGF-β↓, TGF-β1
NF-kB↓,
MIP2↓,
PGE2↓,
NO↓,
Hif1a↓,
VEGFR2/KDR/Flk1↓,
VEGF↓,
MMP2↓,
TIMP2↑,
ITGB1↑,
NCAM↑,
p‑ATM↑,
p‑ATR↑,
p‑CHK1↑,
p‑Chk2↑,
Wnt/(β-catenin)↓,
PI3K↓,
Akt↓,
ERK↓, ERK1/2
cMyc↓,
mTOR↓,
survivin↓,
cMET↓,
EGFR↓,
cycD1/CCND1↓,
cycE1↓,
CDK4/6↓,
p16↑,
p27/CDKN1B↑,
Apoptosis↑,
TumAuto↑,
Ferroptosis↑,
oncosis↑,
TumCCA↑, G0/G1 into M phase, G0/G1 into S phase, G1 and G2/M
ROS↑, ovarian cancer cell line model, artesunate induced oxidative stress, DNA double-strand breaks (DSBs) and downregulation of RAD51 foci
DNAdam↑,
RAD51↓,
HR↓,

2767- Bos,    The potential role of boswellic acids in cancer prevention and treatment
- Review, Var, NA
*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1/CCND1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE/CCNE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1/CCL2↓, LPS-challenged ApoE-/- mice via inhibition of NF-κB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2/PTGS2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/β-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-β-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-β and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoPv↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/β-catenin and NF-κB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-α and IL-1β in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2 pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (Phytosome®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer

6309- Cro,    Crocin exerts anti-tumor effect in colon cancer cells via repressing the JaK pathway
- in-vitro, CRC, HCT116
tumCV↓, while crocin restrained the HCT-116 cells vitality, proliferation and the expression of Ki-67, while inducing apoptosis in a concentration-dependent manner.
TumCP↓,
Ki-67↓,
Apoptosis↓,
Inflam↓, inflammation- and oxidative- related factors in HCT-116 cells were largely blunted by crocin that enhanced ROS, restrained the MMP and suppressed p-JAK2/JAK2, p-STAT3/STAT3, and p-ERK/ERK expression
ROS↑,
MMP↓,
JAK2↓,
STAT3↓,
ERK↓,
MIP2↓, we found that crocin manifested an obvious inhibition of the contents of MIP-2, IL-6, MCP-1, IL-8, IL-1β, and TNF-α in HCT-116 cells in relative to the control group and the inhibitory effect of 200 μM
IL6↓,
MCP1/CCL2↓,
IL8↓,
IL1β↓,
TNF-α↓,
SOD↓, oxidative stress-related factors and confirmed that the contents of SOD, CAT, and GSH in HCT-116 cells were reduced by crocin in relative to the control group and the 200 μM
Catalase↓,
GSH↓,
ROS↑, crocin exhibited a notable increase production of ROS in HCT-116 cells
mtDam↑, crocin is inducing oxidative stress and damaging the mitochondria, leading to cell death.

7140- GI,    Benefits of Ginger and Its Constituent 6-Shogaol in Inhibiting Inflammatory Processes
- Review, Var, NA
*Dose↝, 6-Shogaol is formed from 6-gingerol by dehydration and represents one of the main bioactive principles in dried ginger rhizomes.
*Inflam↓, In vitro and in vivo, 6-shogaol reduced inflammatory mediator systems such as COX-2 or iNOS, affected NFκB and MAPK signaling, and increased levels of cytoprotective HO-1.
*COX2/PTGS2↓,
*iNOS↓,
*NF-kB↓,
*MAPK?,
*HO-1↑,
*PGE2↓, Rat/saline administration 50 and 500 mg/kg extract oral or i.p. Reduced PGE2 serum levels
*TNF-α↓, 25, 50, 100 and 200 mg/kg extract oral Reduced carrageenan-induced paw volume, levels of PGE2, TNF, IL-6, IL-1β, IFNγ, MCP-1, MIP-2, RANTES, and MPO activity and NO levels
*IL6↓,
*IL1β↓,
*IFN-γ↓,
*MCP1/CCL2↓,
*MIP2↓,
*RANTES↓,
*MPO↓,
*NO↓,
*Stroke↓, Therefore, the authors of this study suggest a potential benefit of 6-shogaol for the prevention of stroke [51].
*BrainVol↑, The daily oral administration of 6-shogaol (5 and 20 mg/kg) resulted in protection against transient focal cerebral ischemia, as indicated by a significant reduction of brain infarct volume and production of malondialdehyde (MDA) and of ROS after MCA
*MDA↓,
*ROS↓,
*GSH↑, 6-shoagol treatment resulted in an increased amount of glutathione (GSH) in H2O2-induced HepG2 cells
*NRF2↑, As H2O2-triggered Nrf2 degradation was recovered by 6-shogaol,
*antiOx↑, 6-Shogaol exhibits a stronger antioxidative activity than its homologues
NLRP3↓, 6-shogaol (20 µM) effectively inhibited total protein levels of NLRP3 and pro-IL-1β after a combined LPS and ATP-activated protein up-regulation
HDAC1↓, The LPS-caused induction of HDAC1 protein levels was reduced by 6-shogaol

7780- ISL,    Isoliquiritigenin alleviates LPS/ D-GalN-induced acute liver failure by activating the PGC-1α/ Nrf2 pathway to reduce oxidative stress and inflammatory response
- in-vivo, Nor, NA
*hepatoP↑, ISL significantly improved the liver pathological changes.
*ROS↓, ISL reduced oxidative stress by altering the expression of PGC-1α, Nrf2, HO-1, NQO1, Keap1, GCLC, and GCLM in damaged hepatocytes.
*PGC-1α↝,
*NRF2↑,
*HO-1↑,
*NQO1↝,
*Keap1↝,
*GCLC↝,
*GCLM↝,
*NLRP3↓, NLRP3 inflammasome, IL-1β, IL-6, TNF-α, iNOS, and Mip-2 were repressed by ISL.
*IL1β↓,
*IL6↓,
*TNF-α↓,
*MIP2↓,
*Bax:Bcl2↓, ISL alleviated LPS/D-GalN-induced hepatocytes apoptosis by increasing the Bcl-2/Bax ratio and suppressing the expression of cleaved caspase-3.
*cl‑Casp3↓,
*Inflam↓, ISL improves the ability of anti-oxidative stress, alleviates inflammatory reaction, apoptosis, and inhibits NLRP3 inflammasome
*Apoptosis↓,


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   Ferroptosis↑, 1,   GSH↓, 1,   lipid-P?, 1,   ROS↑, 3,   SOD↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Tf↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,   PPARα↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↓, 1,   Apoptosis↑, 1,   Casp3↑, 1,   Casp8↑, 1,   p‑Chk2↑, 1,   DR4↑, 1,   DR5↑, 1,   Ferroptosis↑, 1,   oncosis↑, 1,   p27/CDKN1B↑, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

p‑ATM↑, 1,   p‑ATR↑, 1,   p‑CHK1↑, 1,   DNAdam↑, 1,   HR↓, 1,   p16↑, 1,   cl‑PARP↑, 1,   RAD51↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   cycE1↓, 1,   p‑RB1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

cMET↓, 1,   ERK↓, 2,   p‑ERK↓, 1,   HDAC1↓, 1,   Let-7↑, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↓, 2,   TOP1↓, 1,   TOP2↑, 1,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

CDK4/6↓, 1,   ITGB1↑, 1,   Ki-67↓, 1,   miR-200b↑, 1,   MMP1↓, 1,   MMP2↓, 2,   MMP9↓, 1,   NCAM↑, 1,   PDGF↓, 1,   TGF-β↓, 1,   TIMP2↑, 1,   TumCI↓, 1,   TumCP↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   EGFR↓, 1,   Hif1a↓, 1,   NO↓, 1,   p‑PDGFR-BB↓, 1,   VEGF↓, 3,   VEGFR2/KDR/Flk1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   CXCR4↓, 1,   IKKα↓, 1,   IL1↓, 1,   IL1α↓, 1,   IL1β↓, 1,   IL6↓, 2,   IL8↓, 1,   Inflam↓, 1,   JAK2↓, 1,   MCP1/CCL2↓, 2,   MIP2↓, 3,   NF-kB↓, 2,   PGE2↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 2,   ChemoSen↑, 1,   Dose↑, 1,   eff↑, 4,   Half-Life↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,   ascitic↓, 1,   EGFR↓, 1,   IL6↓, 2,   Ki-67↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   chemoPv↑, 1,   toxicity↓, 1,  
Total Targets: 105

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   GCLC↝, 1,   GCLM↝, 1,   GSH↑, 1,   HO-1↑, 2,   Keap1↝, 1,   MDA↓, 1,   MPO↓, 1,   NQO1↝, 1,   NRF2↑, 2,   ROS↓, 3,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

PGC-1α↝, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   Apoptosis↓, 1,   Bax:Bcl2↓, 1,   cl‑Casp3↓, 1,   iNOS↓, 1,   MAPK?, 1,   MAPK↑, 1,  

Migration(tgid=13) ⓘ

Ca+2↝, 1,   TGF-β↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IFN-γ↓, 1,   IL1β↓, 2,   IL6↓, 3,   Inflam↓, 4,   MCP1/CCL2↓, 2,   MIP2↓, 3,   NF-kB↓, 3,   PGE2↓, 1,   RANTES↓, 1,   TNF-α↓, 4,  

Synaptic & Neurotransmission(tgid=18) ⓘ

BrainVol↑, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 3,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,   hepatoP↑, 1,   neuroP↑, 1,  
Total Targets: 42

Scientific Paper Hit Count for: MIP2, Macrophage Inflammatory Protein 2
2 Artemisinin
1 Boswellia (frankincense)
1 Crocetin
1 Ginger/6-Shogaol/Gingerol
1 Isoliquiritigenin
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#:788  State#:%  Dir#:1
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