MIP‑1α/CCL3 Cancer Research Results

MIP‑1α/CCL3, C-C Motif Chemokine Ligand 3: Click to Expand ⟱
Source:
Type:
CCL3 (Macrophage Inflammatory Protein-1α, MIP‑1α)

-CCL3 acts as a chemoattractant for various immune cells including NK cells, dendritic cells, and monocytes.

– Its role in tumors can be dual: promoting anti-tumor responses in some contexts while in others, especially through chronic inflammation, it may participate in tumor progression.

CCL3 - C-C Motif Chemokine Ligand 3

Abbreviation: CCL3, MIP-1α

Type: Chemokine / inflammatory cytokine

Function: CCL3 is a CC-family chemokine that signals primarily through CCR1 and CCR5 and regulates recruitment and activation of monocytes, macrophages, lymphocytes, and other immune cells. It plays important roles in inflammatory responses, immune-cell trafficking, and tumor-microenvironment signaling.

Cancer: ↕ Context-dependent. CCL3 can support antitumor immune-cell recruitment in some settings, but elevated CCL3 frequently promotes a pro-inflammatory tumor microenvironment, recruitment of tumor-supportive myeloid cells, angiogenesis, invasion, metastasis, and treatment resistance.

Alzheimer's Disease: ↑ Increased CCL3 is associated with neuroinflammation and activation or recruitment of microglia and other immune cells in Alzheimer's disease and related neurodegenerative models.



Scientific Papers found: Click to Expand⟱
3515- Bor,    EVIDENCE THAT BORON DOWN-REGULATES INFLAMMATION THROUGH THE NF-(KAPPA)B PATHWAY
- in-vitro, Nor, NA
*TNF-α↓, supplemental boron displayed decreased levels of TNF-alpha (a), IL-1ß, MIP-1a, and iNOS expression. Each of these factors is under NF-kappa (k) B control.
*IL1β↓,
*MIP‑1α/CCL3↓,
*iNOS↓,
*NF-kB↓,

7325- GSE,    The Effects of a Grape Seed Procyanidin Extract on Cytochrome P450 3A4 Activity and Inflammatory Mediators in the Lungs of Heavy Active and Former Smokers
- in-vitro, Lung, NA
*cardioP↑, Grape seed procyanidin extract (GSE) is widely used to promote cardiovascular health and has purported anti-inflammatory properties
*Inflam↓,
BioAv↑, leucoselect phytosome (LP), a standardized grape seed procyanidin extract complexed with soy phospholipids to enhance bioavailability, three months of LP treatment
TNF-α↓, and three months of LP treatment significantly decreased tumor necrosis factor (TNF), C-C Motif Chemokine Ligand 3 (CCL3) and granzyme B in BAL fluids.
MIP‑1α/CCL3↓,
GranB/GZMB↓,

7784- ISL,    Isoliquiritigenin attenuates lipopolysaccharide-induced cognitive impairment through antioxidant and anti-inflammatory activity
- in-vivo, AD, NA
*Learn↑, ISL pretreatment reversed these deficits as well as LPS-induced decreases in the hippocampal expression levels of synaptophysin, postsynaptic density-95, brain-derived neurotrophic factor, superoxide dismutase, glutathione peroxidase, and BCL-2.
*PSD95↑,
*BDNF↑,
*SOD↑,
*GPx↑,
*Bcl-2↑,
*SYP↑,
*Bax:Bcl2↓, ISL pretreatment also reversed LPS-induced increases in TUNEL-positive (apoptotic) cells, BAX/BCL-2 ratio, and expression levels of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and C-C motif chemokine ligand 3.
*TNF-α↓,
*IL1β↓,
*IL6↓,
*MIP‑1α/CCL3↓,
*p‑GSK‐3β↑, Pretreatment with ISL increased the expression levels of phosphorylated (p)-GSK-3β, nuclear NRF2, HO-1 mRNA, and NQO1 mRNA, and reversed LPS-induced nuclear translocation of nuclear factor (NF)-κB
*NRF2↑,
*HO-1↑,
*NQO1↑,
*cognitive↑, ISL protects against LPS-induced cognitive impairment and neuronal injury by promoting or maintaining antioxidant capacity and suppressing neuroinflammation, likely through phosphorylation-dependent inactivation of GSK-3β, enhanced expression of NRF
*Inflam↓,

228- MFrot,  MF,    Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
- NA, MS, NA
*CD4+↑, RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4+ cells in the spleen and lymph nodes
*MCP1/CCL2↓, by downregulating the expression of CCL-2, CCL-3 and CCL-5
RANTES↓,
*MIP‑1α/CCL3↓,
*Treg lymp↓, increasing the proportion of Treg cells
*IFN-γ↓, However, on day 20 after immunization, IFN-γ and IL-17A levels in the serum of EAE mice were significantly reduced by the exposure of RMF
*IL17↓,
*CXCc↓, mRNA expression of IFN chemokines (CXCL-1 and CXCL-2), and IL-17 chemokines (CXCL-9 and CXCL-10) had also significantly reduced in EAE mice after RMF exposure.

4861- Uro,    Urolithin A improves Alzheimer's disease cognition and restores mitophagy and lysosomal functions
- in-vivo, AD, NA
*memory↑, Long‐term UA treatment significantly improved learning, memory, and olfactory function in different AD transgenic mice.
*Aβ↓, UA also reduced amyloid beta (Aβ) and tau pathologies and enhanced long‐term potentiation
*toxicity↓, A phase I clinical study confirmed that UA was safe in healthy, sedentary older adults, and that activation of mitochondrial biomarkers in muscle and plasma was observed
*BBB↑, may play a therapeutic role in the brain as it crosses the blood–brain barrier.
*p‑tau↓, UA decreased Aβ accumulation and tau phosphorylation in AD mice
*eff↓, and that the effects disappeared if UA treatment was suspended for 1 month.
*IL1α↓, several proinflammatory cytokines were increased in AD mice and decreased after UA treatment, including Interleukin 1 alpha (IL‐1α), monocyte chemoattractant protein‐1 (MCP‐1)
*MCP1/CCL2↓,
*MIP‑1α/CCL3↓, macrophage inflammatory protein‐1 alpha (MIP‐1α), tumor necrosis factor (TNFα), Interleukin 2 (IL‐2)
*TNF-α↓,
*IL2↓,
*SIRT1↓, UA induced sirtuin expression, mitophagy, and decreased DNA damage
*DNAdam↓,
*Dose↝, UA at doses from 250 to 2000 mg in humans 25 and 1–450 mg/kg in mice 80 has been reported to be safe.
*Strength↑, UA increased muscle strength and physical performance in a 6‐min walk test in elderly humans after 4 months of supplementation.
*motorD↑, Other studies reported that UA improved motor activity in the rotarod test and increased total distance traveled and average speed in the open field test in young C57BL/6J mice 82 and 3xTg AD mice
*CTSZ↓, Ctsz was highly expressed in multiple AD transgenic mouse models, and its expression was normalized by UA treatment


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death(tgid=5)

GranB/GZMB↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

MIP‑1α/CCL3↓, 1,   RANTES↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21)

BioAv↑, 1,  
Total Targets: 5

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0)

Learn↑, 1,   SYP↑, 1,  

Redox & Oxidative Stress(tgid=1)

GPx↑, 1,   HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis(tgid=4)

SIRT1↓, 1,  

Cell Death(tgid=5)

Bax:Bcl2↓, 1,   Bcl-2↑, 1,   iNOS↓, 1,  

DNA Damage & Repair(tgid=10)

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

p‑GSK‐3β↑, 1,  

Migration(tgid=13)

Treg lymp↓, 1,  

Barriers & Transport(tgid=15)

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16)

CD4+↑, 1,   CTSZ↓, 1,   CXCc↓, 1,   IFN-γ↓, 1,   IL17↓, 1,   IL1α↓, 1,   IL1β↓, 2,   IL2↓, 1,   IL6↓, 1,   Inflam↓, 2,   MCP1/CCL2↓, 2,   MIP‑1α/CCL3↓, 4,   NF-kB↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission(tgid=18)

BDNF↑, 1,   PSD95↑, 1,   p‑tau↓, 1,  

Protein Aggregation(tgid=19)

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21)

Dose↝, 1,   eff↓, 1,  

Clinical Biomarkers(tgid=22)

IL6↓, 1,  

Functional Outcomes(tgid=23)

cardioP↑, 1,   cognitive↑, 1,   memory↑, 1,   motorD↑, 1,   Strength↑, 1,   toxicity↓, 1,  
Total Targets: 42

Scientific Paper Hit Count for: MIP‑1α/CCL3, C-C Motif Chemokine Ligand 3
1 Boron
1 Grapeseed extract
1 Isoliquiritigenin
1 Magnetic Field Rotating
1 Magnetic Fields
1 Urolithin
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#:1275  State#:%  Dir#:1
wNotes=on sortOrder:rid,rpid

 

Home Page