RANTES Cancer Research Results

RANTES, CCL5: Click to Expand ⟱
Source:
Type:
RANTES (Regulated on Activation, Normal T Cell Expressed and Secreted), also known as CCL5
• RANTES/CCL5 is a chemokine that plays a central role in recruiting immune cells—such as T cells, eosinophils, and monocytes—to sites of inflammation.
• In the tumor microenvironment, RANTES can influence immune cell infiltration, which may either support anti-tumor responses or, conversely, facilitate a pro-tumorigenic inflammatory milieu depending on the context.
• RANTES is involved in modulating angiogenesis, cell migration, and the deposition of extracellular matrix components. These processes can affect tumor progression and metastasis.

-In several cancer types—including breast, lung, and colorectal cancers—elevated RANTES expression has been associated with more aggressive tumor behavior and, in some instances, poorer prognosis.
Scientific Papers found: Click to Expand⟱
3689- Ash,    Ashwagandha attenuates TNF-α- and LPS-induced NF-κB activation and CCL2 and CCL5 gene expression in NRK-52E cells
- in-vitro, NA, NRK52E
*RenoP↑, ashwaganda WSE as a valid candidate for evaluation of therapeutic potential for the treatment of chronic renal dysfunction.
*NF-kB↓, WSE completely prevented TNF-α-induced increases in CCL5, while attenuating the increase in CCL2 expression and NF-κB activation.
*MCP1/CCL2↓,
*RANTES↓,

2481- Ba,  Rad,    Radiotherapy Increases 12-LOX and CCL5 Levels in Esophageal Cancer Cells and Promotes Cancer Metastasis via THP-1-Derived Macrophages
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, KYSE150
12LOX↓, increased by 12-LOX upregulation but was suppressed by the well-established 12-LOX inhibitor, baicalein
RadioS↑, In prostate cancer cells, 12-LOX inhibition has been shown to increase radiation sensitivity,
Dose↝, Additionally, 12-LOX expression was significantly inhibited at 40 µmol/L
RANTES↓, post-radiotherapy protein levels of CCL5 increased in Eca109 and Kyse150 cells but were inhibited by baicalein
MCP1/CCL2↓, Baicalein, a recognized inhibitor of 12-LOX, successfully inhibited CCL2 and CCL5 expression, which was verified by RT-qPCR.

7137- GI,    6-Shogaol from dried ginger inhibits growth of prostate cancer cells both in vitro and in vivo through inhibition of STAT3 and NF-κB signaling
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - vitro+vivo, Pca, HMVP2
STAT3↓, Mechanistic studies revealed that 6-SHO reduced constitutive and interleukin (IL)-6-induced STAT3 activation and inhibited both constitutive and TNF-α-induced NF-κB activity in these cells.
TNF-α↓,
NF-kB↓,
cycD1/CCND1↓, 6-SHO decreased the level of several STAT3 and NF-κB-regulated target genes at the protein level, including cyclin D1, survivin, and cMyc
survivin↓,
cMyc↓,
IL7↓, modulated mRNA levels of chemokine, cytokine, cell cycle, and apoptosis regulatory genes (IL-7, CCL5, BAX, BCL2, p21, and p27)
RANTES↓, 6-SHO decreased the mRNA expression of IL-7 and CCL5 in both DU145 and LNCaP cells.
BAX↑,
Bcl-2↓,
P21↑, 6-SHO increased the expression of p21, p27, SOCS1 and IRF1
p27/CDKN1B↑,
SOCS1↑,
IRF1↑,
eff↑, these results demonstrate that 6-GIN and 6-PAR have the ability to block growth and reduce survival of both human and mouse PCa cells but that they are both less potent than 6-SHO
TumVol↓, treatment with 6-SHO produced statistically significant decreases in tumor volume at both the 50 and 100 mg/kg doses (62% and 73%, respectively; p<0.05)
TumW↓, tumor weights were also reduced at both doses of 6-SHO (48% and 65% reduction, respectively)
toxicity↓, Taken together, these data demonstrate that 6-SHO has potent in vivo antitumor activity at the doses tested and is free of apparent adverse effects.

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

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.

4036- NAD,  VitB3,    NAD+ supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency
- in-vivo, AD, NA
*Inflam↓, NAD+ supplementation with nicotinamide riboside significantly normalized neuroinflammation, synaptic transmission, phosphorylated Tau, and DNA damage as well as improved learning and memory and motor function.
*p‑tau↓, NR Decreases Tau Phosphorylation but Not Aβ Accumulation in AD and AD/Polβ Mice.
*DNAdam↓,
*memory↑,
*motorD↑,
*cognitive↑, NR improved cognitive function in multiple behavioral tests and restored hippocampal synaptic plasticity in 3xTgAD mice and 3xTgAD/Polβ+/− mice.
*BBB↑, NR enters the brain and boosts cellular NAD+ levels when administered orally.
IL1β↓, AD/Polβ mice had elevated levels of proinflammatory cytokines and chemokines, including IL-1α, TNFα, MCP-1, IL-1β, MIP-1α, and RANTES, and decreased levels of antiinflammatory cytokines such as IL-10 (Fig. 3G and Fig. S4A). NR treatment normalized
*TNF-α↓,
*MCP1/CCL2↓,
*RANTES↓,
*ROS↓, NR treatment of AD fibroblasts resulted in decreased levels of mitochondrial ROS compared with vehicle-treated cells
*SIRT3↑, NR Treatment Decreases DNA Damage and Apoptosis Through SIRT3 and SIRT6.
*SIRT6↑,

3012- RosA,  Rad,    Rosmarinic Acid Prevents Radiation-Induced Pulmonary Fibrosis Through Attenuation of ROSMYPT1TGFβ1 Signaling Via miR-19b-3p
- in-vitro, Nor, IMR90
*Inflam↓, RA reduced X-ray-induced the expression of inflammatory related factors, and the level of reactive oxygen species.
*ROS↓,
*p‑NF-kB↓, RA down-regulated the phosphorylation of nuclear factor kappa-B (NF-κB).
*Rho↓, RA attenuated RhoA/Rock signaling through upregulating miR-19b-3p, leading to the inhibition of fibrosis
*ROCK1↓,
*radioP↑, RA attenuated radiation- induced damage by its capacity to relieve inflammation and regulate inflammatory factors.
*MCP1/CCL2↓, RA treatment reduced RNA levels of NF-kB target gene, including MCP-1, RANTES, and ICAM-1
*RANTES↓,
*ICAM-1↓,
*PGC1A↑, Western blot analysis showed that RA promoted the expression of PGC-1a and reduced the expression of NOX-4, this evidence further suggested that RA inhibits the generation of ROS
*NOX4↓,
*Dose↝, RA exerted strongly protective effects in the X-ray-induced inflammation at doses of 60 mg/kg, and treat- ment with a higher dose (120 mg/kg) do not enhance its anti- inflammatory effect.


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

IL7↓, 1,   IRF1↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

12LOX↓, 1,   cMyc↓, 1,  

Cell Death(tgid=5) ⓘ

BAX↑, 1,   Bcl-2↓, 1,   p27/CDKN1B↑, 1,   survivin↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,  

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

HDAC1↓, 1,   STAT3↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   MCP1/CCL2↓, 1,   NF-kB↓, 1,   RANTES↓, 3,   SOCS1↑, 1,   TNF-α↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,   eff↑, 1,   RadioS↑, 1,  

Functional Outcomes(tgid=23) ⓘ

toxicity↓, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 25

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   GSH↑, 1,   HO-1↑, 1,   MDA↓, 1,   MPO↓, 1,   NOX4↓, 1,   NRF2↑, 1,   ROS↓, 3,   SIRT3↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PGC1A↑, 1,  

Cell Death(tgid=5) ⓘ

iNOS↓, 1,   MAPK?, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,   SIRT6↑, 1,  

Migration(tgid=13) ⓘ

Rho↓, 1,   ROCK1↓, 1,   Treg lymp↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2/PTGS2↓, 1,   CXCc↓, 1,   ICAM-1↓, 1,   IFN-γ↓, 2,   IL17↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 3,   MCP1/CCL2↓, 5,   MIP‑1α/CCL3↓, 1,   MIP2↓, 1,   NF-kB↓, 2,   p‑NF-kB↓, 1,   PGE2↓, 1,   RANTES↓, 4,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

BrainVol↑, 1,   p‑tau↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 2,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,   memory↑, 1,   motorD↑, 1,   radioP↑, 1,   RenoP↑, 1,  
Total Targets: 46

Scientific Paper Hit Count for: RANTES, CCL5
2 Radiotherapy/Radiation
2 Ginger/6-Shogaol/Gingerol
1 Ashwagandha(Withaferin A)
1 Baicalein
1 Magnetic Field Rotating
1 Magnetic Fields
1 nicotinamide adenine dinucleotide
1 Vitamin B3,Niacin
1 Rosmarinic acid
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#:1221  State#:%  Dir#:1
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