SOCS1 Cancer Research Results

SOCS1, suppressor of cytokine signaling 1: Click to Expand ⟱
Source: CGL-Driver Genes
Type: TSG
SOCS1 (Suppressor of Cytokine Signaling 1) is a protein that plays a critical role in regulating the immune response and cellular signaling pathways. It is part of the SOCS family of proteins, which are known to inhibit cytokine signaling and modulate various cellular processes, including cell growth, differentiation, and apoptosis.
SOCS1 is often considered a tumor suppressor because it can inhibit pathways that promote cell proliferation and survival, such as the JAK/STAT signaling pathway. Dysregulation of this pathway is commonly observed in various cancers.
In many cancers, SOCS1 expression is found to be downregulated or silenced. This can occur through mechanisms such as promoter methylation, histone modifications, or genetic mutations. The loss of SOCS1 expression can lead to unchecked activation of signaling pathways, particularly the JAK/STAT pathway, which is associated with increased cell proliferation and survival.
Scientific Papers found: Click to Expand⟱
573- ART/DHA,    Artesunate suppresses tumor growth and induces apoptosis through the modulation of multiple oncogenic cascades in a chronic myeloid leukemia xenograft mouse model
- vitro+vivo, NA, NA
p‑p38↓,
p‑ERK↓,
p‑CREB↓,
p‑Chk2↓,
p‑STAT5↓,
p‑RSK↓,
SOCS1↑,
Apoptosis↑,
Casp3↑,

424- CUR,    Curcumin inhibits autocrine growth hormone-mediated invasion and metastasis by targeting NF-κB signaling and polyamine metabolism in breast cancer cells
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231
Src↓,
p‑STAT1↓, pSTAT-1
p‑Akt↓,
p‑p44↓, p-p44
p‑p42↓, p-p42
RAS↓,
Raf↓, c-RAF
Vim↓,
β-catenin/ZEB1↓,
P53↓,
Bcl-2↓,
Mcl-1↓,
PIAS-3↑,
SOCS-3↑,
SOCS1↑,
ROS↑,
NF-kB↓, NF-kB inactivation, ROS generation and PA depletion in MCF-7, MDA-MB-453 and MDA-MB-231 breast can- cer cells
PAO↑,
SSAT↑,
P21↑,
Bak↑,

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.

3359- QC,    Quercetin modifies 5′CpG promoter methylation and reactivates various tumor suppressor genes by modulating epigenetic marks in human cervical cancer cells
- in-vitro, Cerv, HeLa
DNMTs↓, When nuclear extracts were incubated with increasing doses of quercetin (25 and 50uM) they were found to inhibit the function of the DNMTs by 32% and 49% respectively, in comparison to untreated control
HDAC↓, quercetin (25 and 50 uM), they were found to inhibit the function of the HDACs by 47% and 62% in comparison to untreated control.
HMTs↓, quercetin (25 and 50 uM), were found to inhibit the function of the HMT H3K9 by 63% and 71%
DNMT3A↓, preferred binding of quercetin on DNMT3A and DNMT3B is within the substrate binding cavity and could competitively inhibit the protein
EZH2↓, Quercetin interacts with EZH2 and functions as an inhibitor
HDAC1↓, Quercetin was able to reduce the activity of class II HDACs significantly, with concomitant downregulation of HDAC1, HDAC2, HDAC6, HDAC7, and HDAC11 expression
HDAC2↓,
HDAC6↓,
HDAC11↓,
G9a↓, quercetin and this correlates well with the observed downregulation of G9A expression
TIMP3↑, Fig8: quercetin resulted in reduced promoter methylation of several TSGs (APC, CDH1, CDH13, DAPK1, FHIT, GSTP1, MGMT, MLH1, PTEN, RARB, RASSF1, SOC51, TIMP3, and VHL
PTEN↑,
SOCS1↑,


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:


NA, unassigned(tgid=0) ⓘ

IL7↓, 1,   IRF1↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

PAO↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

p‑p42↓, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,   p‑CREB↓, 1,   SSAT↑, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 2,   Casp3↑, 1,   p‑Chk2↓, 1,   Mcl-1↓, 1,   p27/CDKN1B↑, 1,   p‑p38↓, 1,   p‑RSK↓, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

EZH2↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNMT3A↓, 1,   DNMTs↓, 1,   G9a↓, 1,   P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   P21↑, 2,  

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

p‑ERK↓, 1,   HDAC↓, 1,   HDAC1↓, 1,   HDAC11↓, 1,   HDAC2↓, 1,   HDAC6↓, 1,   HMTs↓, 1,   PIAS-3↑, 1,   PTEN↑, 1,   RAS↓, 1,   Src↓, 1,   p‑STAT1↓, 1,   STAT3↓, 1,   p‑STAT5↓, 1,  

Migration(tgid=13) ⓘ

p‑p44↓, 1,   TIMP3↑, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NF-kB↓, 2,   RANTES↓, 1,   SOCS-3↑, 1,   SOCS1↑, 4,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EZH2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

toxicity↓, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 56

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: SOCS1, suppressor of cytokine signaling 1
1 Artemisinin
1 Curcumin
1 Ginger/6-Shogaol/Gingerol
1 Quercetin
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#:288  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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