TumCI Cancer Research Results

TumCI, Tumor Cell invasion: Click to Expand ⟱
Source:
Type:
Tumor cell invasion is a critical process in cancer progression and metastasis, where cancer cells spread from the primary tumor to surrounding tissues and distant organs. This process involves several key steps and mechanisms:

1.Epithelial-Mesenchymal Transition (EMT): Many tumors originate from epithelial cells, which are typically organized in layers. During EMT, these cells lose their epithelial characteristics (such as cell-cell adhesion) and gain mesenchymal traits (such as increased motility). This transition is crucial for invasion.

2.Degradation of Extracellular Matrix (ECM): Tumor cells secrete enzymes, such as matrix metalloproteinases (MMPs), that degrade the ECM, allowing cancer cells to invade surrounding tissues. This degradation facilitates the movement of cancer cells through the tissue.

3.Cell Migration: Once the ECM is degraded, cancer cells can migrate. They often use various mechanisms, including amoeboid movement and mesenchymal migration, to move through the tissue. This migration is influenced by various signaling pathways and the tumor microenvironment.

4.Angiogenesis: As tumors grow, they require a blood supply to provide nutrients and oxygen. Tumor cells can stimulate the formation of new blood vessels (angiogenesis) through the release of growth factors like vascular endothelial growth factor (VEGF). This not only supports tumor growth but also provides a route for cancer cells to enter the bloodstream.

5.Invasion into Blood Vessels (Intravasation): Cancer cells can invade nearby blood vessels, allowing them to enter the circulatory system. This step is crucial for metastasis, as it enables cancer cells to travel to distant sites in the body.

6.Survival in Circulation: Once in the bloodstream, cancer cells must survive the immune response and the shear stress of blood flow. They can form clusters with platelets or other cells to evade detection.

7.Extravasation and Colonization: After traveling through the bloodstream, cancer cells can exit the circulation (extravasation) and invade new tissues. They may then establish secondary tumors (metastases) in distant organs.

8.Tumor Microenvironment: The surrounding microenvironment plays a significant role in tumor invasion. Factors such as immune cells, fibroblasts, and signaling molecules can either promote or inhibit invasion and metastasis.


IBD, Inflammatory Bowel Disease: Click to Expand ⟱
Inflammatory Bowel Disease

The main pathways involved in IBD include intestinal barrier dysfunction, mucus barrier impairment, dysbiosis-driven innate immune activation, and persistent cytokine-mediated inflammation. Key barrier components such as ZO-1, occludin, claudins, and MUC2 are commonly disrupted, increasing epithelial permeability and microbial translocation. This promotes activation of inflammatory hubs including TNF-α, NF-κB, IL-1β, IL-6/STAT3, and IL-23/Th17, while JAK/STAT signaling integrates multiple cytokine inputs that sustain chronic mucosal injury. Together, these pathways drive epithelial damage, immune dysregulation, and failure of mucosal healing in ulcerative colitis and Crohn’s disease

Rank Pathway / Axis Representative Targets / Markers Typical Direction in IBD Main Relevance
1 Intestinal Barrier Integrity / Tight Junctions ZO-1 (TJP1), Occludin (OCLN), Claudins (especially CLDN2, CLDN1) ZO-1 ↓, OCLN ↓, barrier loosened; CLDN2 often ↑ Core barrier failure increases intestinal permeability, microbial entry, and chronic inflammation
2 Mucus Barrier / Goblet Cell Axis MUC2, goblet cells, antimicrobial peptides MUC2 and goblet protection often impaired Weak mucus defense exposes the epithelium to luminal bacteria and antigens
3 TNF-α Inflammatory Axis TNF-α, TNFR1, TNFR2 Major inflammatory driver and validated therapeutic target in IBD
4 NF-κB Signaling NF-κB, IKK, IκB, COX-2, iNOS Central transcriptional hub for cytokines, chemokines, and inflammatory amplification
5 IL-23 / Th17 Axis IL-23, IL-23R, IL-17A, IL-22, RORγt ↑ / dysregulated Important bridge between innate and adaptive immune inflammation
6 JAK / STAT Signaling JAK1, JAK2, TYK2, STAT3 ↑ / activated Integrates multiple cytokine signals that sustain mucosal inflammation
7 IL-6 / STAT3 Axis IL-6, IL-6R, gp130, STAT3 Supports inflammatory persistence, immune-cell survival, and epithelial injury signaling
8 IL-1β / Inflammasome Axis IL-1β, NLRP3, ASC, caspase-1 Promotes innate inflammation, cytokine escalation, and epithelial damage
9 Microbiota / Dysbiosis / PRR Signaling Dysbiosis, TLRs, MyD88, LPS-related signaling Dysregulated / activated Links altered microbiota to barrier loss and immune activation
10 Oxidative Stress / Redox Imbalance ROS, lipid peroxidation, MPO, antioxidant defenses ↑ oxidative stress Contributes to epithelial injury, inflammatory signaling, and impaired healing
11 Leukocyte Trafficking / Adhesion Integrins, MAdCAM-1, ICAM-1, VCAM-1, chemokines Drives immune-cell recruitment into inflamed intestinal tissue
12 Epithelial Apoptosis / Restitution / Mucosal Healing Caspases, repair pathways, epithelial proliferation and restitution markers Injury ↑, healing impaired Determines whether mucosal damage resolves or progresses to chronic disease
Rank Natural Product Best Fit in IBD Evidence Level Main Rationale Notes
1 Curcumin Mainly Ulcerative Colitis (UC) Best human evidence Strongest overall adjunctive clinical support among common natural products for active UC Anti-inflammatory; NF-κB / cytokines / oxidative stress; mucosal support
2 Indigo naturalis (Qing Dai) Mainly UC Strong efficacy, safety-limited Good human efficacy signals, but safety concerns lower practical rank Anti-colitic; immune/inflammatory modulation; use caution flag for safety
3 Boswellia serrata UC / colitis Older smaller human trials Suggestive remission data and anti-inflammatory relevance, but evidence base is limited 5-LOX / leukotrienes / inflammation / mucosal protection
4 Aloe vera gel Mild-to-moderate UC Small human trial signal Some human improvement signal, though not as strong as curcumin or indigo naturalis Mucosal soothing / anti-inflammatory / healing support
5 Andrographis paniculata / andrographolide Mostly UC Mixed human, stronger preclinical Mechanistically promising, but human benefit is less consistent NF-κB / cytokines / barrier and anti-inflammatory support
6 Carvacrol Experimental colitis / dysbiosis / barrier dysfunction Preclinical Promising anti-colitis terpene with anti-inflammatory, antioxidant, and microbiota-related effects Dysbiosis / intestinal barrier integrity / NF-κB / oxidative stress
7 Thymol Experimental colitis / barrier dysfunction Preclinical Promising anti-colitis terpene with cytokine suppression and NF-κB-related effects Dysbiosis / intestinal barrier integrity / NF-κB / COX-2 / oxidative stress
8 Carvacrol + Thymol Experimental colitis, dysbiosis, bile-acid modulation Preclinical, mechanistically strong Combination may be especially relevant due to microbiota and bile-acid pathway effects in DSS colitis Bifidobacterium / secondary bile acids / barrier support / anti-colitic signaling
9 Peppermint oil Supportive / experimental colitis / GI symptom relief Mainly preclinical for IBD; stronger IBS evidence Menthol-rich oil with anti-inflammatory, antispasmodic, and possible barrier-supportive effects, but limited direct human IBD evidence Menthol / TRP modulation / cytokines / oxidative stress / GI symptom support


Scientific Papers found: Click to Expand⟱
2674- BBR,    Berberine: A novel therapeutic strategy for cancer
- Review, Var, NA - Review, IBD, NA
Inflam↓, AntiCan↑, Apoptosis↑, TumAuto↑, TumCCA↑, TumMeta↓, TumCI↓, eff↑, eff↑, CD4+↓, TNF-α↓, IL1↓, BioAv↓, BioAv↓, other↓, AMPK↑, MAPK↓, NF-kB↓, IL6↓, MCP1↓, PGE2↓, COX2↓, *ROS↓, *antiOx↑, *GPx↑, *Catalase↑, AntiTum↑, TumCP↓, angioG↓, Fas↑, FasL↑, ROS↑, ATM↑, P53↑, RB1↑, Casp9↑, Casp8↑, Casp3↓, BAX↑, Bcl-2↓, Bcl-xL↓, IAP1↓, XIAP↓, survivin↓, MMP2↓, MMP9↓, CycB/CCNB1↓, CDC25↓, CDC25↓, Cyt‑c↑, MMP↓, RenoP↑, mTOR↓, MDM2↓, LC3II↑, ERK↓, COX2↓, MMP3↓, TGF-β↓, EMT↑, ROCK1↓, FAK↓, RAS↓, Rho↓, NF-kB↓, uPA↓, MMP1↓, MMP13↓, ChemoSen↑,

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:


Redox & Oxidative Stress

ROS↑, 1,  

Mitochondria & Bioenergetics

CDC25↓, 2,   MMP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis

AMPK↑, 1,  

Cell Death

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↓, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Fas↑, 1,   FasL↑, 1,   IAP1↓, 1,   MAPK↓, 1,   MDM2↓, 1,   survivin↓, 1,  

Transcription & Epigenetics

other↓, 1,  

Autophagy & Lysosomes

LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair

ATM↑, 1,   P53↑, 1,  

Cell Cycle & Senescence

CycB/CCNB1↓, 1,   RB1↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

EMT↑, 1,   ERK↓, 1,   mTOR↓, 1,   RAS↓, 1,  

Migration

FAK↓, 1,   MMP1↓, 1,   MMP13↓, 1,   MMP2↓, 1,   MMP3↓, 1,   MMP9↓, 1,   Rho↓, 1,   ROCK1↓, 1,   TGF-β↓, 1,   TumCI↓, 1,   TumCP↓, 1,   TumMeta↓, 1,   uPA↓, 1,  

Angiogenesis & Vasculature

angioG↓, 1,  

Immune & Inflammatory Signaling

CD4+↓, 1,   COX2↓, 2,   IL1↓, 1,   IL6↓, 1,   Inflam↓, 1,   MCP1↓, 1,   NF-kB↓, 2,   PGE2↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance

BioAv↓, 2,   ChemoSen↑, 1,   eff↑, 2,  

Clinical Biomarkers

IL6↓, 1,  

Functional Outcomes

AntiCan↑, 1,   AntiTum↑, 1,   RenoP↑, 1,  
Total Targets: 61

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   ROS↓, 1,  
Total Targets: 4

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
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:58  Cells:%  prod#:%  Target#:324  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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