CLDN3 Cancer Research Results

CLDN3, claudin‑3: Click to Expand ⟱
Source:
Type:
Claudin-3 is a member of the claudin family of proteins, which are integral components of tight junctions in epithelial cells. Tight junctions are crucial for maintaining the integrity of epithelial barriers, regulating paracellular permeability, and facilitating cell signaling.
Claudin-3, in particular, has been studied for its role in various cancers, and its expression levels can have significant implications for tumor behavior and patient prognosis.
Role of Claudin-3
Tight Junction Formation: Claudin-3 is involved in the formation of tight junctions, which help to maintain cell polarity and barrier function in epithelial tissues. It plays a role in regulating the permeability of the epithelial barrier.
Cell Signaling: Beyond its structural role, claudin-3 can participate in signaling pathways that influence cell proliferation, differentiation, and apoptosis.
Expression Patterns:
Overexpression: Claudin-3 is often found to be overexpressed in various cancers, including breast cancer, ovarian cancer, and pancreatic cancer. This overexpression can contribute to tumor progression and metastasis.
Loss of Expression: In some contexts, loss of claudin-3 expression can also be observed, particularly in more aggressive tumor types. This loss can disrupt tight junction integrity and promote invasiveness.


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?,


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Immune & Inflammatory Signaling

IL1β↓, 1,  

Synaptic & Neurotransmission

ADAM10?, 1,  

Functional Outcomes

Risk↓, 1,  
Total Targets: 3

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: CLDN3, claudin‑3
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#:61  State#:%  Dir#:2
wNotes=on sortOrder:rid,rpid

 

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