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.


Scientific Papers found: Click to Expand⟱
1123- aLinA,    Linoleic acid induces an EMT-like process in mammary epithelial cells MCF10A
- in-vitro, BC, NA - in-vitro, NA, MCF10
TumCP↑, Linoleic acid (LA) induces proliferation and invasion in breast cancer cells.
E-cadherin↓,
Snail↑, increase of Snail1, Snail2, Twist1, Twist2 and Sip1 expressions.
Twist↑,
ZEB2↑,
FAK↑,
NF-kB↑,
MMP2↓, Furthermore, LA induces FAK and NFκB activation, MMP-2 and -9 secretions, migration and invasion.
MMP9↓,
*EMT↑, LA promotes an EMT-like process in MCF10A
TumCI↑,

5204- CAP,    Low-concentration capsaicin promotes colorectal cancer metastasis by triggering ROS production and modulating Akt/mTOR and STAT-3 pathways
- in-vitro, Colon, SW480 - in-vitro, Colon, CT26
TumCP↓, high-concentration of capsaicin (≥ 200 µM for SW480 and CT-26 cell lines; ≥ 25 µM for HCT116 cell line) inhibited CRC cell proliferation in a dose-dependent manner
TumCMig↑, low-concentration of capsaicin (100 µM for SW480 and CT-26 cell lines; 12.5 µM for HCT116 cell line) enhanced both migratory and invasive capability of these cells
TumCI↑,
EMT↑, 100 µM capsaicin induced epithelial-to-mesenchymal (EMT), up-regulated expression of MMP-2 and MMP-9, and activated Akt/mTOR and STAT-3 pathways in SW480 cells.
MMP2↓,
MMP9↑,
STAT3↑,
TumMeta↑, capsaicin-induced metastasis of CRC cells was mediated by modulating reactive oxygen species (ROS) production.
ROS↑,

4565- TQ,    Thymoquinone in the clinical treatment of cancer: Fact or fiction?
- Review, BC, NA
Dose↝, high performance liquid chromatography of the seeds oil of N. sativa revealed that TQ may attain up to 27.8% of the volatile oil (w/w) composition.
TumCCA↑, It was shown to induce G1/S cell cycle arrest by up-regulating p21WAF1/Cip1[19] or p27Kip1[20] and down-regulating cyclin D1[21] and was reported to control invasion and metastasis of cancer.
P21↑,
cycD1/CCND1↓,
TumCI↑,
TumMeta↓,
Bcl-2↓, down-regulate PPAR-γ related genes, including Bcl-2, Bcl-xL and survivin at both mRNA and protein expression levels in MCF-7 cells.
Bcl-xL↓,
survivin↓,
PTEN↑, TQ induces apoptosis in doxorubicin-resistant breast cancer cells through the up-regulation of phosphatase and tensin homolog (PTEN) at the transcription level.
Akt↓, The up-regulated PTEN, in turn, inhibits the phosphatidylinositol-3 kinase/Akt pathway and induces p53 and p21 protein expression
P53↑,
NF-kB↓, Inhibition of NF-κB by TQ increases apoptosis in hyperplastic stages of tumor development and decreases proliferation at least in part by reducing CyclinD1 expression, which inhibits mammary tumor progression.
cardioP↑, TQ has an antioxidant protective effect against the doxorubicin-induced cardiotoxicity
Dose↝, Patients with breast cancer were under treatment for 2 weeks with 400 mg/day. The authors reported neither toxicity nor therapeutic response.

1222- Z,    Zinc regulates primary ovarian tumor growth and metastasis through the epithelial to mesenchymal transition
- in-vitro, Ovarian, NA
EMT↑, zinc contributes to ovarian tumor metastasis by promoting EMT through a MTF-1 dependent pathway
TumCMig↑,
TumCI↑,
ERK↑,
Akt↑, .


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,  

Cell Death

Akt↓, 1,   Akt↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   survivin↓, 1,  

DNA Damage & Repair

P53↑, 1,  

Cell Cycle & Senescence

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

Proliferation, Differentiation & Cell State

EMT↑, 2,   ERK↑, 1,   PTEN↑, 1,   STAT3↑, 1,  

Migration

E-cadherin↓, 1,   FAK↑, 1,   MMP2↓, 2,   MMP9↓, 1,   MMP9↑, 1,   Snail↑, 1,   TumCI↑, 4,   TumCMig↑, 2,   TumCP↓, 1,   TumCP↑, 1,   TumMeta↓, 1,   TumMeta↑, 1,   Twist↑, 1,   ZEB2↑, 1,  

Immune & Inflammatory Signaling

NF-kB↓, 1,   NF-kB↑, 1,  

Drug Metabolism & Resistance

Dose↝, 2,  

Functional Outcomes

cardioP↑, 1,  
Total Targets: 32

Pathway results for Effect on Normal Cells:


Proliferation, Differentiation & Cell State

EMT↑, 1,  
Total Targets: 1

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
1 alpha Linolenic acid
1 Capsaicin
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:%  Cells:%  prod#:%  Target#:324  State#:%  Dir#:2
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