MUC1 Cancer Research Results

MUC1, Mucin 1: Click to Expand ⟱
Source:
Type: oncoprotein
The mucin 1 (MUC1) heterodimeric oncoprotein is overexpressed in human prostate cancers with aggressive pathologic and clinical features, resulting in a poor MUC1 (Mucin 1) is a glycoprotein that is expressed on the surface of epithelial cells and plays a role in cell signaling, protection, and lubrication. It is also involved in various biological processes, including cell adhesion and immune response outcome.
MUC1 is often overexpressed in various types of cancers, including breast, ovarian, pancreatic, and colorectal cancers.
Scientific Papers found: Click to Expand⟱
5932- CAR,    Carvacrol attenuates mucosal barrier impairment and tumorigenesis by regulating gut microbiome
- in-vivo, IBD, NA - in-vivo, Park, NA
*GutMicro↑, Carvacrol can regulate the gut microbiota. bundance of specific microbiota, such as Lactobacillus, Escherichia coli/Shigella, and Lachnoclostridium.
Risk↓, Carvacrol inhibits the development of colitis-associated colorectal cancer.
*Inflam↓, nti-inflammatory and antioxidant traits,
*antiOx↓,
*ZO-1↑, carvacrol significantly restored colonic length (p < 0.01) and re-established key tight junction proteins like ZO-1.
*iNOS↓, downregulated mRNA levels of inflammatory mediators such as iNOS and IL-6.
*IL6↓,
*NO↓, carvacrol has been shown to suppress nitric oxide and prostaglandin E2 production
*PGE2↓,
*memory↑, carvacrol improves memory deficits in Parkinson’s disease models
*TLR4↓, anti-inflammatory effects of carvacrol by inhibiting the TLR4/NF-κB signaling pathway
*NF-kB↓,
*IBI↑, Carvacrol improves intestinal barrier function
*CLDN3↑, expression levels of ZO-1, Claudin3, Claudin1, Occludin, and Mucin were significantly increased in the carvacrol group compared to the DSS group
*CLDN1↑,
*MUC1↑,
*OCLN↑,
*iNOS↑, carvacrol significantly inhibited the mRNA expression levels of iNOS, COX-2, Interferon-γ, IL-1β, and IL-6 in the intestinal tracts of colitis mice
*COX2↓,
*IFN-γ↓,
IL1β↓,
ADAM10?,

1575- statins,  Citrate,    Inhibition of Lung Cancer Growth: ATP Citrate Lyase Knockdown and Statin Treatment Leads to Dual Blockade of Mitogen-Activated Protein Kinase (MAPK) and Phosphatidylinositol-3-Kinase (PI3K)/AKT Pathways
- in-vitro, NSCLC, A549
eff↑, we find that statins, inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which act downstream of ACL in the cholesterol synthesis pathway, dramatically enhance the anti-tumor effects of ACL inhibition, even regressing tumors
HMG-CoA↓, statins, inhibitors of (HMG-CoA) reductase
eff↑, statins dramatically enhance the anti-tumor effects of ACL inhibition
AntiTum↑,
EGFR↓, reduce the growth of EGF receptor
eff↑, ACL knockdown cells, H2O2 induced more apoptosis, which was further amplified with statin treatment (Fig. 1I). These data suggest that oxidant stress can tip ACL knockdown cells into apoptosis and that statin treatment magnifies this effect.
ROS↑, suggesting involvement of reactive oxygen species (ROS) in the induction of apoptosis by PI3K inhibitors.
EMT↓, Reversal of EMT
E-cadherin↑, increase in E-cadherin
MUC1↑, Mucin staining in ACL knockdown tumors is markedly increased, further suggesting that differentiation is induced in this condition
p‑ACLY↓, Statin treatment downregulates the phosphorylation of ACL and AKT
p‑Akt↓,
eff↑, . In A549 cells, Na-citrate supplementation caused a slight downregulation of AKT phosphorylation


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 ⓘ

ROS↑, 1,  

Core Metabolism/Glycolysis ⓘ

p‑ACLY↓, 1,   HMG-CoA↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   MUC1↑, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,  

Synaptic & Neurotransmission ⓘ

ADAM10?, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 4,  

Clinical Biomarkers ⓘ

EGFR↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   Risk↓, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,  

Cell Death ⓘ

iNOS↓, 1,   iNOS↑, 1,  

Migration ⓘ

CLDN1↑, 1,   MUC1↑, 1,   ZO-1↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

CLDN3↑, 1,   IBI↑, 1,   OCLN↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IFN-γ↓, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TLR4↓, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,  
Total Targets: 20

Scientific Paper Hit Count for: MUC1, Mucin 1
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

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