ZO-1 Cancer Research Results

ZO-1, Zonula occludens-1: Click to Expand ⟱
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ZO-1 (Zonula occludens-1) is a protein that plays a crucial role in the formation and maintenance of tight junctions in epithelial cells. Tight junctions are essential for maintaining the integrity of epithelial barriers and regulating the passage of ions and molecules across the cell membrane.

In the context of cancer, ZO-1 has been implicated in several ways:

1.Loss of ZO-1 expression: Reduced or lost expression observed in various types of cancer.
2.Disruption of tight junctions: Cancer cells often exhibit disrupted tight junctions, which can lead to increased permeability and the loss of epithelial barrier function. ZO-1 is a key component of tight junctions, and its disruption can contribute to the development and progression of cancer.
3.Epithelial-to-mesenchymal transition (EMT): ZO-1 has been shown to play a role in regulating EMT, a process by which epithelial cells acquire a mesenchymal phenotype. EMT is a key event in the development of cancer metastasis, and ZO-1's role in regulating this process is an area of active research.
4.Tumor suppressor function: ZO-1 has been proposed to have tumor suppressor functions, and its loss or downregulation can contribute to the development of cancer. ZO-1's tumor suppressor functions may be related to its ability to regulate cell growth, apoptosis, and cell migration.

ZO-1 generally acts as a tumor suppressor by maintaining epithelial integrity. In many cancers, downregulation or mislocalization of ZO-1 is observed and is associated with a poorer prognosis due to the facilitation of EMT and metastasis.
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
2617- Ba,    Potential of baicalein in the prevention and treatment of cancer: A scientometric analyses based review
- Review, Var, NA
Ca+2↑, MMP2↓, MMP9↓, Vim↓, Snail↓, E-cadherin↑, Wnt↓, β-catenin/ZEB1↓, p‑Akt↓, p‑mTOR↓, NF-kB↓, i-ROS↑, Bcl-2↓, BAX↑, Cyt‑c↑, Casp3↑, Casp9↑, STAT3↓, IL6↓, MMP2↓, MMP9↓, NOTCH↓, PPARγ↓, p‑NRF2↓, HK2↓, LDHA↓, PDK1↓, Glycolysis↓, PTEN↑, Akt↓, Hif1a↓, MMP↓, VEGF↓, VEGFR2↓, TOP2↓, uPA↓, TIMP1↓, TIMP2↓, cMyc↓, TrxR↓, ASK1↑, Vim↓, ZO-1↑, E-cadherin↑, SOX2↓, OCT4↓, Shh↓, Smo↓, Gli1↓, N-cadherin↓, XIAP↓,
2919- LT,    Luteolin as a potential therapeutic candidate for lung cancer: Emerging preclinical evidence
- Review, Var, NA
RadioS↑, ChemoSen↑, chemoP↑, *lipid-P↓, *Catalase↑, *SOD↑, *GPx↑, *GSTs↑, *GSH↑, *TNF-α↓, *IL1β↓, *Casp3↓, *IL10↑, NRF2↓, HO-1↓, NQO1↓, GSH↓, MET↓, p‑MET↓, p‑Akt↓, HGF/c-Met↓, NF-kB↓, Bcl-2↓, SOD2↓, Casp8↑, Casp3↑, PARP↑, MAPK↓, NLRP3↓, ASC↓, Casp1↓, IL6↓, IKKα↓, p‑p65↓, p‑p38↑, MMP2↓, ICAM-1↓, EGFR↑, p‑PI3K↓, E-cadherin↓, ZO-1↑, N-cadherin↓, CLDN1↓, β-catenin/ZEB1↓, Snail↓, Vim↑, ITGB1↓, FAK↓, p‑Src↓, Rac1↓, Cdc42↓, Rho↓, PCNA↓, Tyro3↓, AXL↓, CEA↓, NSE↓, SOD↓, Catalase↓, GPx↓, GSR↓, GSTs↓, GSH↓, VitE↓, VitC↓, CYP1A1↓, cFos↑, AR↓, AIF↑, p‑STAT6↓, p‑MDM2↓, NOTCH1↓, VEGF↓, H3↓, H4↓, HDAC↓, SIRT1↓, ROS↑, DR5↑, Cyt‑c↑, p‑JNK↑, PTEN↓, mTOR↓, CD34↓, FasL↑, Fas↑, XIAP↓, p‑eIF2α↑, CHOP↑, LC3II↑, PD-1↓, STAT3↓, IL2↑, EMT↓, cachexia↓, BioAv↑, *Half-Life↝, *eff↑,
5934- TV,    Protective Effects of Natural Antioxidants on Inflammatory Bowel Disease: Thymol and Its Pharmacological Properties
- Review, Var, NA
*Inflam↓, *antiOx↑, *Bacteria↓, AntiTum↑, *toxicity∅, *IBI↑, *ZO-1↑, *OCLN↑, *COX1↑, *TLR4↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *TAC↑, *NRF2↑, *GutMicro↑,
1740- VitD3,    Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms
- Review, Var, NA
Risk↓, eff↑, eff↑, Risk↓, Risk↓, ChemoSen↑, RadioS↑, Cyt‑c↑, Casp3↑, Casp9↑, hTERT/TERT↓, eff↑, E-cadherin↑, CLDN2↑, ZO-1↑, Snail↓, Zeb1↓, Vim↓, VEGF↓, NK cell↑, Risk↓, eff↑,

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 ⓘ

Catalase↓, 1,   CYP1A1↓, 1,   GPx↓, 1,   GSH↓, 2,   GSR↓, 1,   GSTs↓, 1,   HO-1↓, 1,   NQO1↓, 1,   NRF2↓, 1,   p‑NRF2↓, 1,   ROS↑, 1,   i-ROS↑, 1,   SOD↓, 1,   SOD2↓, 1,   TrxR↓, 1,   VitC↓, 1,   VitE↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   MMP↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   LDHA↓, 1,   PDK1↓, 1,   PPARγ↓, 1,   SIRT1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 2,   ASK1↑, 1,   BAX↑, 1,   Bcl-2↓, 2,   Casp1↓, 1,   Casp3↑, 3,   Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 3,   DR5↑, 1,   Fas↑, 1,   FasL↑, 1,   HGF/c-Met↓, 1,   hTERT/TERT↓, 1,   p‑JNK↑, 1,   MAPK↓, 1,   p‑MDM2↓, 1,   p‑p38↑, 1,  

Transcription & Epigenetics ⓘ

H3↓, 1,   H4↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   p‑eIF2α↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,  

DNA Damage & Repair ⓘ

PARP↑, 1,   PCNA↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD34↓, 1,   cFos↑, 1,   EMT↓, 1,   Gli1↓, 1,   HDAC↓, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   p‑PI3K↓, 1,   PTEN↓, 1,   PTEN↑, 1,   Shh↓, 1,   Smo↓, 1,   SOX2↓, 1,   p‑Src↓, 1,   STAT3↓, 2,   p‑STAT6↓, 1,   TOP2↓, 1,   Wnt↓, 1,  

Migration ⓘ

AXL↓, 1,   Ca+2↑, 1,   Cdc42↓, 1,   CEA↓, 1,   CLDN1↓, 1,   CLDN2↑, 1,   E-cadherin↓, 1,   E-cadherin↑, 3,   FAK↓, 1,   ITGB1↓, 1,   MET↓, 1,   p‑MET↓, 1,   MMP2↓, 3,   MMP9↓, 2,   N-cadherin↓, 2,   Rac1↓, 1,   Rho↓, 1,   Snail↓, 3,   TIMP1↓, 1,   TIMP2↓, 1,   Tyro3↓, 1,   uPA↓, 1,   Vim↓, 3,   Vim↑, 1,   Zeb1↓, 1,   ZO-1↑, 3,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

EGFR↑, 1,   Hif1a↓, 1,   VEGF↓, 3,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↓, 1,   ICAM-1↓, 1,   IKKα↓, 1,   IL2↑, 1,   IL6↓, 2,   NF-kB↓, 2,   NK cell↑, 1,   p‑p65↓, 1,   PD-1↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 2,   eff↑, 4,   RadioS↑, 2,  

Clinical Biomarkers ⓘ

AR↓, 1,   CEA↓, 1,   EGFR↑, 1,   hTERT/TERT↓, 1,   IL6↓, 2,   NSE↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   cachexia↓, 1,   chemoP↑, 1,   Risk↓, 4,  
Total Targets: 130

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSTs↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   SOD↑, 1,   TAC↑, 1,  

Cell Death ⓘ

Casp3↓, 1,  

Migration ⓘ

ZO-1↑, 1,  

Barriers & Transport ⓘ

IBI↑, 1,   OCLN↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↑, 1,   IL10↑, 1,   IL1β↓, 2,   Inflam↓, 1,   NF-kB↓, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,  

Functional Outcomes ⓘ

toxicity∅, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 25

Scientific Paper Hit Count for: ZO-1, Zonula occludens-1
1 Baicalein
1 Luteolin
1 Thymol-Thymus vulgaris
1 Vitamin D3
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:26  Cells:%  prod#:%  Target#:674  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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