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.
GBM, Glioblastoma: Click to Expand ⟱
Glioblastoma is a fast-growing and aggressive brain tumor.
Scientific Papers found: Click to Expand⟱
1157- And,    Andrographolide suppresses the migratory ability of human glioblastoma multiforme cells by targeting ERK1/2-mediated matrix metalloproteinase-2 expression
- in-vitro, GBM, GBM8401 - in-vitro, GBM, U251
TumCI↓, TumCMig↓, MMP2↓, ERK↝,
2700- BBR,    Cell-specific pattern of berberine pleiotropic effects on different human cell lines
- in-vitro, GBM, U343 - in-vitro, GBM, MIA PaCa-2 - in-vitro, Nor, HDFa
selectivity↑, TumCCA↑, Casp3↑, TumCI↓, TumCMig↓, N-cadherin?, DNMT1↑,
2757- BetA,    Betulinic Acid Inhibits Glioma Progression by Inducing Ferroptosis Through the PI3K/Akt and NRF2/HO-1 Pathways
- in-vitro, GBM, U251
tumCV↓, TumCMig↓, TumCI↓, Apoptosis↑, p‑PI3K↓, p‑Akt↓, Ferroptosis↑, HO-1↑, NRF2↑,
5885- CAR,    Inhibition of TRPM7 by carvacrol suppresses glioblastoma cell proliferation, migration and invasion
- in-vitro, GBM, U87MG - in-vitro, Nor, HEK293
TRPM7↓, tumCV↓, TumCMig↓, TumCI↓, MMP2↓, toxicity↓, *Inflam↓, AntiDiabetic↑, cardioP↑, neuroP↑, selectivity↑, Apoptosis↑, p‑Cofilin↑, F-actin↓, PI3K↓, Akt↓, MEK↓, MAPK↓,
5912- CAR,    Inhibition of TRPM7 by carvacrol suppresses glioblastoma cell proliferation migration and invasion
- in-vitro, GBM, U87MG - in-vitro, Nor, HEK293
TRPM7↓, tumCV↓, TumCMig↓, TumCI↓, MMP2↓, p‑Cofilin↑, RAS↓, MEK↓, MAPK↓, PI3K↓, Akt↓,
4489- Chit,  SeNPs,    Inhibiting Metastasis and Improving Chemosensitivity via Chitosan-Coated Selenium Nanoparticles for Brain Cancer Therapy
- in-vitro, GBM, U87MG
TumCG↓, TumCMig↓, TumCI↓, ChemoSen↑, *BBB↑, eff↑, eff↑, eff↑, selectivity↑, MMP2↓, MMP9↓, EPR↑,
2590- CHr,    Chrysin suppresses proliferation, migration, and invasion in glioblastoma cell lines via mediating the ERK/Nrf2 signaling pathway
- in-vitro, GBM, T98G - in-vitro, GBM, U251 - in-vitro, GBM, U87MG
TumCP↓, TumCMig↓, TumCI↓, NRF2↓, HO-1↓, NADPH↓, ERK↓,
2511- H2,    Molecular hydrogen suppresses glioblastoma growth via inducing the glioma stem-like cell differentiation
- in-vivo, GBM, U87MG
TumCG↓, OS↑, CD133↓, Ki-67↓, angioG↓, Diff↑, TumCMig↓, TumCI↓, Dose↝, BBB↑, mt-ROS↑,
1153- HNK,    Honokiol Eliminates Glioma/Glioblastoma Stem Cell-Like Cells via JAK-STAT3 Signaling and Inhibits Tumor Progression by Targeting Epidermal Growth Factor Receptor
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG - in-vivo, NA, NA
tumCV↓, Apoptosis↑, TumCMig↓, TumCI↓, Bcl-2↓, EGFR↓, CD133↓, Nestin↓, Akt↓, ERK↓, Casp3↑, p‑STAT3↓, TumCG↓,
516- MFrot,  immuno,  MF,    Anti-tumor effect of innovative tumor treatment device OM-100 through enhancing anti-PD-1 immunotherapy in glioblastoma growth
- vitro+vivo, GBM, U87MG
TumCP↓, Apoptosis↑, TumCMig↓, ROS↑, PD-L1↑, TumVol↓, eff↑, *toxicity∅, eff↑, *toxicity∅, Dose↝, tumCV↓, TumCI↓,
1911- Nos,    Noscapine inhibits tumor growth in TMZ-resistant gliomas
- in-vitro, GBM, NA - in-vivo, GBM, NA
TumCG↓, TumCI↓, OS↑,
2127- TQ,    Therapeutic Potential of Thymoquinone in Glioblastoma Treatment: Targeting Major Gliomagenesis Signaling Pathways
- Review, GBM, NA
chemoP↑, ChemoSen↑, BioAv↑, PTEN↑, PI3K↓, Akt↓, TumCCA↓, NF-kB↓, p‑Akt↓, p65↓, XIAP↓, Bcl-2↓, COX2↓, VEGF↓, mTOR↓, RAS↓, Raf↓, MEK↓, ERK↓, MMP2↓, MMP9↓, TumCMig↓, TumCI↓, Casp↑, cl‑PARP↑, ROS⇅, ROS↑, MMP↓, eff↑, Telomerase↓, DNAdam↑, Apoptosis↑, STAT3↓, RadioS↑,
961- Z,    Zinc Downregulates HIF-1α and Inhibits Its Activity in Tumor Cells In Vitro and In Vivo
- in-vitro, RCC, RCC4 - vitro+vivo, GBM, U373MG - in-vitro, Nor, HUVECs
Hif1a↓, HIF-1↓, VEGF↓, TumCI↓,

Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   HO-1↓, 1,   HO-1↑, 1,   NRF2↓, 1,   NRF2↑, 1,   ROS↑, 2,   ROS⇅, 1,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MEK↓, 3,   MMP↓, 1,   Raf↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

NADPH↓, 1,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 2,   Apoptosis↑, 5,   Bcl-2↓, 2,   Casp↑, 1,   Casp3↑, 2,   Ferroptosis↑, 1,   MAPK↓, 2,   Telomerase↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 5,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 2,   Diff↑, 1,   ERK↓, 3,   ERK↝, 1,   mTOR↓, 1,   Nestin↓, 1,   PI3K↓, 3,   p‑PI3K↓, 1,   PTEN↑, 1,   RAS↓, 2,   STAT3↓, 1,   p‑STAT3↓, 1,   TRPM7↓, 2,   TumCG↓, 4,  

Migration ⓘ

p‑Cofilin↑, 2,   F-actin↓, 1,   Ki-67↓, 1,   MMP2↓, 5,   MMP9↓, 2,   N-cadherin?, 1,   TumCI↓, 13,   TumCMig↓, 11,   TumCP↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   EPR↑, 1,   HIF-1↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,   p65↓, 1,   PD-L1↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 2,   Dose↝, 2,   eff↑, 6,   RadioS↑, 1,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   Ki-67↓, 1,   PD-L1↑, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 1,   chemoP↑, 1,   neuroP↑, 1,   OS↑, 2,   toxicity↓, 1,   TumVol↓, 1,  
Total Targets: 78

Pathway results for Effect on Normal Cells:


Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

toxicity∅, 2,  
Total Targets: 3

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
2 Carvacrol
1 Andrographis
1 Berberine
1 Betulinic acid
1 chitosan
1 Selenium NanoParticles
1 Chrysin
1 Hydrogen Gas
1 Honokiol
1 Magnetic Field Rotating
1 immunotherapy
1 Magnetic Fields
1 Noscapine
1 Thymoquinone
1 Zinc
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:27  Cells:%  prod#:%  Target#:324  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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