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.
NPC, Nasopharyngeal Carcinoma (NPC): Click to Expand ⟱
Nasopharyngeal carcinoma, or nasopharynx cancer, is the most common cancer originating in the nasopharynx, most commonly in the postero-lateral nasopharynx or pharyngeal recess, accounting for 50% of cases.
Nasopharyngeal carcinoma (NPC) is a type of cancer that originates in the epithelial cells lining the nasopharynx, which is the upper part of the throat located behind the nose and above the soft palate.
-(NPC) is a malignant tumor which is commonly found in East Asia and Africa.
Scientific Papers found: Click to Expand⟱
4820- ASTX,    Astaxanthin suppresses the malignant behaviors of nasopharyngeal carcinoma cells by blocking PI3K/AKT and NF-κB pathways via miR-29a-3p
- in-vitro, NPC, NA
TumCP↓, TumCI↓, Apoptosis↑, TumCCA↑, cycD1/CCND1↓, Bcl-2↓, P21↑, BAX↑, PI3K↓, Akt↓, NF-kB↓, miR-29b↑,
4685- EGCG,    Epigallocathechin gallate, polyphenol present in green tea, inhibits stem-like characteristics and epithelial-mesenchymal transition in nasopharyngeal cancer cell lines
- in-vitro, NPC, TW01 - in-vitro, NPC, TW06
CSCs↓, EMT↓, TumCMig↓, TumCI↓, OCT4↓, Snail↓, Vim↓, E-cadherin↓, HSP70/HSPA5↓, HSP90↓, AntiTum↓,
2360- SK,    Shikonin inhibits growth, invasion and glycolysis of nasopharyngeal carcinoma cells through inactivating the phosphatidylinositol 3 kinase/AKT signal pathway
- in-vitro, NPC, HONE1 - in-vitro, NPC, SUNE-1
TumCP↓, Apoptosis↑, TumCMig↓, TumCI↓, GlucoseCon↓, lactateProd↓, ATP↓, PKM2↓, PI3K↓, Akt↓, MMP3↓, MMP9↓, TIMP1↑,
4856- Uro,    Study on the biological mechanism of urolithin a on nasopharyngeal carcinoma in vitro
- in-vitro, NPC, CNE1 - in-vitro, NPC, CNE2
Apoptosis↑, MMP↓, ROS↑, E-cadherin↑, BAX↑, cl‑Casp3↑, PARP↑, MMP2↓, MMP9↓, N-cadherin↓, Vim↓, Snail↓, eff↓, TumCP↓, TumCMig↓, TumCI↓, EMT↓,

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 ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↓, 1,   lactateProd↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 3,   BAX↑, 2,   Bcl-2↓, 1,   cl‑Casp3↑, 1,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↓, 1,   HSP90↓, 1,  

DNA Damage & Repair ⓘ

PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 2,   OCT4↓, 1,   PI3K↓, 2,  

Migration ⓘ

E-cadherin↓, 1,   E-cadherin↑, 1,   miR-29b↑, 1,   MMP2↓, 1,   MMP3↓, 1,   MMP9↓, 2,   N-cadherin↓, 1,   Snail↓, 2,   TIMP1↑, 1,   TumCI↓, 4,   TumCMig↓, 3,   TumCP↓, 3,   Vim↓, 2,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,  

Functional Outcomes ⓘ

AntiTum↓, 1,  
Total Targets: 37

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
1 Astaxanthin
1 EGCG (Epigallocatechin Gallate)
1 Shikonin
1 Urolithin
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:67  Cells:%  prod#:%  Target#:324  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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