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.
Ovarian, Ovarian Cancer: Click to Expand ⟱
Ovarian Cancer
Scientific Papers found: Click to Expand⟱
722- Bor,    Boric acid as a promising agent in the treatment of ovarian cancer: Molecular mechanisms
- in-vitro, Ovarian, MDAH-2774
TumCP↓, TumCI↓, TumCMig↓, Apoptosis↑, ROS↑, miR-21↓, miR-130a↓, Casp8∅, Casp10∅, cycD1/CCND1∅, CDK6∅, CDK4∅, FADD∅, DR4∅, DR5∅,
5941- Cela,    Celastrol inhibits migration and invasion through blocking the NF-κB pathway in ovarian cancer cells
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, OVCAR-3
TumCMig↓, TumCI↓, NF-kB↓, p65↓, MMP9↓, eff↑, AntiTum↑, Inflam↓, AntiDiabetic↑,
1247- EMD,    Emodin exerts antitumor effects in ovarian cancer cell lines by preventing the development of cancer stem cells via epithelial mesenchymal transition
- vitro+vivo, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S
TumCP↓, TumCMig↓, TumCI↓, EMT↓, N-cadherin↓, Vim↓, E-cadherin↑, TumCG↓, CD133↓, OCT4↓, CSCs↓,
3500- MF,    Moderate Static Magnet Fields Suppress Ovarian Cancer Metastasis via ROS-Mediated Oxidative Stress
- in-vitro, Ovarian, SKOV3
ROS↑, CSCs↓, CD44↓, SOX2↓, cMyc↓, TumMeta↓, TumCI↓, TumCMig↓, CD133↓, Nanog↓,
1237- PTS,    Pterostilbene induces cell apoptosis and inhibits lipogenesis in SKOV3 ovarian cancer cells by activation of AMPK-induced inhibition of Akt/mTOR signaling cascade
- in-vitro, Ovarian, SKOV3
TumCMig↓, TumCI↓, MDA↑, ROS↑, BAX↑, Casp3↑, Bcl-2↓, SREBP1↓, FASN↓, AMPK↓, p‑AMPK↑, p‑P53↑, p‑TSC2↑, p‑Akt↓, p‑mTOR↓, p‑S6K↓, p‑4E-BP1↓,
5127- Sal,    Salinomycin repressed the epithelial–mesenchymal transition of epithelial ovarian cancer cells via downregulating Wnt/β-catenin pathway
- in-vitro, Ovarian, NA
TumCI↓, E-cadherin↑, N-cadherin↓, Vim↓, Wnt↓, β-catenin/ZEB1↓, TumCP↓, TumCMig↓, EMT↓,

Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

MDA↑, 1,   ROS↑, 3,  

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,   p‑AMPK↑, 1,   cMyc↓, 1,   FASN↓, 1,   p‑S6K↓, 1,   SREBP1↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp10∅, 1,   Casp3↑, 1,   Casp8∅, 1,   DR4∅, 1,   DR5∅, 1,   FADD∅, 1,  

Kinase & Signal Transduction ⓘ

p‑TSC2↑, 1,  

Transcription & Epigenetics ⓘ

miR-21↓, 1,  

DNA Damage & Repair ⓘ

p‑P53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4∅, 1,   cycD1/CCND1∅, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑4E-BP1↓, 1,   CD133↓, 2,   CD44↓, 1,   CSCs↓, 2,   EMT↓, 2,   p‑mTOR↓, 1,   Nanog↓, 1,   OCT4↓, 1,   SOX2↓, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration ⓘ

E-cadherin↑, 2,   miR-130a↓, 1,   MMP9↓, 1,   N-cadherin↓, 2,   TumCI↓, 6,   TumCMig↓, 6,   TumCP↓, 3,   TumMeta↓, 1,   Vim↓, 2,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,   p65↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6∅, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   AntiTum↑, 1,  
Total Targets: 51

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
1 Boron
1 Celastrol
1 Emodin
1 Magnetic Fields
1 Pterostilbene
1 salinomycin
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:20  Cells:%  prod#:%  Target#:324  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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