TJ Cancer Research Results

TJ, Tight junctions: Click to Expand ⟱
Source: HalifaxProj(promote)
Type:
Tight junctions (TJ) are specialized structures that form a barrier between epithelial cells, regulating the passage of substances between the cells and maintaining the integrity of tissue. They play a crucial role in maintaining cell polarity, tissue homeostasis, and the selective permeability of epithelial layers.

1.Overexpression of some claudins (e.g., claudin-1, -3, -4) in certain cancers is often associated with increased tumor aggressiveness and poor prognosis (protumor effects).
2.Downregulation or mislocalization of occludin and ZO proteins is generally linked to loss of cell–cell adhesion, EMT, and worse outcomes.
3.In contrast, loss of claudin-7 can remove its tumor suppressor functions, thereby facilitating invasion.

The expression and impact of tight junction components in cancer is an area of active research—each protein can have dual roles (protumor or tumor suppressive) based on the tumor type, the molecular context, and the stage of disease progression.
Scientific Papers found: Click to Expand⟱
7012- Fuc,    Fucoidan: A promising natural therapeutic agent for protecting human kidney health
- Review, EC, NA
*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.

7006- Fuc,    Seaweeds in the Oncology Arena: Anti-Cancer Potential of Fucoidan as a Drug—A Review
- Review, Var, NA
*toxicity↓, Fucoidan is a versatile, nontoxic marine-origin heteropolysaccharide that has received much attention due to its beneficial biological properties and safety.
*AntiViral↑, ucoidan has been demonstrated to exhibit a variety of conventional bioactivities, such as antiviral, antioxidant, and immune-modulatory characteristics, and anticancer activity against a wide range of malignancies has also recently been discovered.
*antiOx↑,
*Imm⇅,
AntiCan↑,
TumCCA↑, Fucoidan inhibits tumorigenesis by prompting cell cycle arrest and apoptosis, blocking metastasis and angiogenesis, and modulating physiological signaling molecules.
Apoptosis↑,
TumMeta↓,
angioG↓,
antiNeop↑, Fucoidans’ capacity to bind to Toll-like receptors and intervene with the action of vascular endothelial growth factors (VEGF) and matrix metalloproteinases (MMPs) could explain their anti-neoplastic properties
VEGF↓,
MMPs↓,
BioAv↑, Low molecular weight fractions (LMWF), in particular, are thought to be more biocompatible [47]
BioAv↑, in rats, following topical administration of fucoidan (MW 750 kDa) from Fucus vesiculosus demonstrated fine skin-penetrating characteristics.
ROS⇅, Induction/inhibition of reactive oxygen species (ROS), mitochondrial instability, and caspase and poly (ADP-ribose) polymerase (PARP) cleavage are all aspects of it
cl‑PARP↑, fucoidan treatment causes PARP cleavage and caspase-3/7 activation in MCF-7 cells, which are hallmarks of apoptosis [
Casp3↑,
Casp7↑,
ROS↑, human hepatoma SMMC-7721 cells, fucoidan therapy caused noteworthy growth inhibition and ROS-mediated apoptosi
GSH↓, lower glutathione consumption (GSH), mitochondrial swelling, and depolarization of the mitochondrial membrane potential
MMP↓,
PI3K↓, Fucoidan inhibits PI3K, suppressing ERK and activates MAPK, limiting cancer cell proliferation and decreasing Bcl-2 to Bax ratio, inducing caspase-dependent apoptosis in BEL-7402 and LM3 cell lines
ERK↓,
MAPK↑,
TumCP↓,
Bax:Bcl2↑,
TJ↑, Meanwhile, dietary fucoidan progressively restores intestinal villi by upregulating the expression of tight junction proteins such as ZO-1, Occludin, Claudin-1, and Claudin-8 via p38 MAPK and ERK1/2 activation.
ZO-1↑,
OCLN↑,
CLDN1↑,
IBI↑, fucoidan supplementation improves intestinal barrier function by enhancing intestinal microbiota diversity
GutMicro↑,
NK cell↑, ↑NK cell-mediated anticancer immunity
STAT3↓, Inhibits STAT3 Signaling
eff↑, Astragalus polysaccharide as a topical mucosal adjuvant to boost the anticancer efficacy of immune checkpoint inhibitors

7035- GA,    Gallic acid attenuates LPS-induced inflammation in Caco-2 cells by suppressing the activation of the NF-κB/MAPK signaling pathway
- in-vitro, IBD, Caco-2
*Inflam↓, Gallic acid (GA) is renowned for its remarkable biological activity, encompassing anti-inflammatory and antioxidant properties.
*antiOx↑,
*CLDN1↓, Our findings demonstrate that 5 μg/mL GA restores the downregulation of the mRNA and protein levels of Claudin-1, Occludin, and ZO-1 and decreases the expressions of inflammatory factors such as IL-6, IL-1β and TNF-α induced by LPS.
*OCLN↓,
*ZO-1↓,
*IL6↓,
*IL1β↓,
*TNF-α↓,
*BAX↓, downregulating the mRNA levels of pro-apoptotic factors ( Bax, Bad, Caspase-3, Caspase-8, and Caspase-9)
*BAD↓,
*Casp3↓,
*Casp8↓,
*ROS↓, GA also reduces the levels of reactive oxygen species increased by LPS and restores the activity of antioxidant enzymes, namely, superoxide dismutase and catalase, as well as the level of glutathione.
*SOD↑,
*Catalase↑,
*GSH↑,
*TJ↑, GA increases the expressions of tight junction proteins, reduces cell apoptosis, relieves oxidative stress and suppresses the activation of the NF-κB/MAPK pathway
*Apoptosis↓,
*NF-kB↓,
*MAPK↓,

7903- IVT,    Inhibition of advanced glycation end products by Isovitexin alleviates intestinal damage: Toward dietary strategies for gut health
- in-vivo, Nor, NA
*AGEs↓, Results demonstrated that ISV effectively inhibited AGEs formation in bovine serum albumin (BSA)-
*TAC↑, In C. elegans, ISV reduced AGEs accumulation, enhanced antioxidant capacity, and improved intestinal barrier function.
*IBI↑,
*TJ↑, upregulated tight junction proteins, and suppressed oxidative stress and apoptosis.
*ROS↓,
*Apoptosis↓,


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:


Redox & Oxidative Stress(tgid=1) ⓘ

GSH↓, 1,   ROS↑, 1,   ROS⇅, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Bax:Bcl2↑, 1,   Casp3↑, 1,   Casp7↑, 1,   MAPK↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

ERK↓, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

CLDN1↑, 1,   MMPs↓, 1,   TJ↑, 1,   TumCP↓, 1,   TumMeta↓, 1,   ZO-1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,   OCLN↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NK cell↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   antiNeop↑, 1,  
Total Targets: 30

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Buty↑, 1,   diuretic↑, 1,   GLP-1R↑, 1,   SCFAs↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 2,   GPx↑, 1,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 3,   SOD↑, 2,   TAC↑, 1,   uricA↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↓, 2,   BAD↓, 1,   BAX↓, 1,   Casp3↓, 1,   Casp8↓, 1,   MAPK↓, 2,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

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

ERK↑, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

CLDN1↓, 1,   COL1↓, 1,   Fibrosis↓, 1,   RAGE↓, 1,   TGF-β1↓, 1,   TJ↑, 3,   ZO-1↓, 1,   α-SMA↓, 1,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 2,   OCLN↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

HMGB1↓, 1,   IL1β↓, 1,   IL6↓, 1,   Imm⇅, 1,   Inflam↓, 2,   JAK2↓, 1,   NF-kB↓, 2,   TNF-α↓, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 1,   GutMicro↑, 1,   IL6↓, 1,   RAGE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

RenoP↑, 1,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,  
Total Targets: 58

Scientific Paper Hit Count for: TJ, Tight junctions
2 Fucoidan
1 Gallic acid
1 Isovitexin
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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