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.
PC, Pancreatic Cancer: Click to Expand ⟱
Pancreatic Cancer: Hypoxia (low oxygen tension) is commonly found in solid tumors. Hypoxia-inducible factor-1 (HIF-1),is a key mediator of the cellular response to hypoxia and is overexpressed in a wide variety of solid tumors, including pancreatic cancer.
Nanog is highly expressed in CSCs compared to normal cells [93–97]
HIF-1↑
Scientific Papers found: Click to Expand⟱
5260- 3BP,    Systemic Delivery of Microencapsulated 3-Bromopyruvate for the Therapy of Pancreatic Cancer
- in-vivo, PC, NA
TumCG↓, toxicity↓, BioAv↝, GAPDH↓, toxicity↑, Dose↝, ATP↓, eff↑, TumCI↓, MMP9↓, toxicity↓,
5637- BCA,  ATV,    Combination Treatment of Biochanin A and Atorvastatin Alters Mitochondrial Bioenergetics, Modulating Cell Metabolism and Inducing Cell Cycle Arrest in Pancreatic Cancer Cells
- in-vitro, PC, AsPC-1 - in-vitro, PC, PANC1 - in-vitro, PC, MIA PaCa-2
eff↑, TumCI↓, STAT3↓, Apoptosis↑,
5510- bemA,    Combined inhibition of ACLY and CDK4/6 reduces cancer cell growth and invasion
- in-vitro, BC, MDA-MB-231 - in-vitro, PC, NA
eff↑, Apoptosis↑, TumCI↓, ACLY↓, LDL↓, eff↑, TumCP↓,
5688- BJ,    Brucea Javanica Oil Emulsion Injection inhibits proliferation of pancreatic cancer via regulating apoptosis-related genes
- vitro+vivo, PC, MIA PaCa-2
TumCG↓, TumCI↓, TumCCA↑, Apoptosis↑, BAX↑, cl‑Casp3↑, Bcl-2↓, MMP2↓, BACE↓, TOP2↓,
1423- Bos,    Acetyl-11-keto-β-Boswellic Acid Suppresses Invasion of Pancreatic Cancer Cells Through The Downregulation of CXCR4 Chemokine Receptor Expression
- in-vitro, Melanoma, U266 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, SkBr3 - in-vitro, PC, PANC1
CXCR4↓, TumCI↓, HER2/EBBR2↓, NF-kB↓,
6073- CHL,  GEM,    Chlorophyllin exerts synergistic anti-tumor effect with gemcitabine in pancreatic cancer by inducing cuproptosis
- in-vitro, PC, NA
ChemoSen↑, eff↑, AntiTum↑, TumCP↓, TumCI↓, TumCMig↓, Apoptosis↑, GSH↓, ROS↑, HSP70/HSPA5↑,
11- CUR,    Curcumin inhibits hypoxia-induced epithelial‑mesenchymal transition in pancreatic cancer cells via suppression of the hedgehog signaling pathway
- in-vitro, PC, PANC1
HH↓, Shh↓, Smo↓, Gli1↓, N-cadherin↓, E-cadherin↑, Vim↓, TumCP↓, TumCMig↓, TumCI↓, EMT↓, chemoPv↑,
476- CUR,    The effects of curcumin on proliferation, apoptosis, invasion, and NEDD4 expression in pancreatic cancer
- in-vitro, PC, PATU-8988 - in-vitro, PC, PANC1
TumCMig↓, TumCI↓, Apoptosis↑, NEDD9↓, p‑Akt↓, p‑mTOR↓, PTEN↑, p73↑, β-TRCP↑,
19- Deg,    Deguelin inhibits proliferation and migration of human pancreatic cancer cells in vitro targeting hedgehog pathway
- in-vitro, PC, Bxpc-3 - in-vitro, PC, PANC1
HH↓, Gli1↓, PTCH1↓, Sufu↓, MMP2↓, MMP9↓, PI3K/Akt↓, HIF-1↓, VEGF↓, IKKα↓, NF-kB↓, EMT↓, AMPK↑, mTOR↓, survivin↓, TumCG↓, Apoptosis↑, TumCMig↓, TumCI↓,
22- EGCG,    Inhibition of sonic hedgehog pathway and pluripotency maintaining factors regulate human pancreatic cancer stem cell characteristics
- in-vitro, PC, CD133+ - in-vitro, PC, CD44+ - in-vitro, PC, CD24+ - in-vitro, PC, ESA+
HH↓, Smo↓, PTCH1↓, PTCH2↓, Gli1↓, GLI2↓, Gli↓, Bcl-2↓, XIAP↓, Shh↓, survivin↓, Casp3↑, Casp7↑, CSCs↓, Nanog↓, cMyc↓, OCT4↓, EMT↓, Snail↓, Slug↓, Zeb1↓, TumCMig↓, TumCI↓, eff↑,
688- EGCG,  GEM,    Epigallocatechin-3-Gallate (EGCG) Suppresses Pancreatic Cancer Cell Growth, Invasion, and Migration partly through the Inhibition of Akt Pathway and Epithelial–Mesenchymal Transition: Enhanced Efficacy When Combined with Gemcitabine
- in-vitro, PC, NA
Zeb1↓, β-catenin/ZEB1↓, Vim↓, Akt↓, p‑IGFR↓, TumCG↓, TumCMig↓, TumCI↓,
1186- Gb,    Ginkgolic acid suppresses the development of pancreatic cancer by inhibiting pathways driving lipogenesis
- in-vitro, PC, NA - in-vitro, Nor, HUVECs - in-vivo, PC, NA
tumCV↓, *toxicity∅, TumCMig↓, TumCI↓, Apoptosis↑, AMPK↑, lipoGen↓, ACC↓, FASN↓,
2881- HNK,    Honokiol Suppressed Pancreatic Cancer Progression via miR-101/Mcl-1 Axis
- in-vitro, PC, PANC1
tumCV↓, Casp3↑, Apoptosis↑, TumCCA↑, TumCI↓, Mcl-1↓, EMT↓,
2882- HNK,    Honokiol Suppresses Perineural Invasion of Pancreatic Cancer by Inhibiting SMAD2/3 Signaling
- in-vitro, PC, PANC1
TumCI↓, TumCMig↓, p‑SMAD2↓, p‑SMAD3↓, EMT↓, N-cadherin↓, Vim↓, E-cadherin↑, Snail↓, Slug↓, Rho↓, ROCK1↓,
974- JG,    Juglone down-regulates the Akt-HIF-1α and VEGF signaling pathways and inhibits angiogenesis in MIA Paca-2 pancreatic cancer in vitro
- in-vitro, PC, MIA PaCa-2
Hif1a↓, VEGF↓, p‑Akt↓, TumCP↓, TumCI↓,
4520- MAG,    Magnolol Suppresses Pancreatic Cancer Development In Vivo and In Vitro via Negatively Regulating TGF-β/Smad Signaling
- vitro+vivo, PC, PANC1
Vim↓, E-cadherin↑, EMT↓, N-cadherin↓, p‑SMAD2↓, p‑SMAD3↓, TumCP↓, TumCMig↓, TumCI↓, TGF-β↓,
4976- Nimb,    Nimbolide inhibits pancreatic cancer growth and metastasis through ROS-mediated apoptosis and inhibition of epithelial-to-mesenchymal transition
- vitro+vivo, PC, NA
ROS↑, Apoptosis↑, TumAuto↑, TumCP↓, TumCMig↓, TumCI↓, EMT↓, Dose↓, selectivity↑, Akt↓, eff↓, BAX↑, cl‑Casp3↑, cl‑PARP↑, Bcl-2↓,
1225- OLST,    Orlistat Induces Ferroptosis in Pancreatic Neuroendocrine Tumors by Inactivating the MAPK Pathway
- vitro+vivo, PC, NA
TumCMig↓, TumCI↓, Ferroptosis↑, MAPK↓,
56- QC,    Quercetin inhibits epithelial–mesenchymal transition, decreases invasiveness and metastasis, and reverses IL-6 induced epithelial–mesenchymal transition, expression of MMP by inhibiting STAT3 signaling in pancreatic cancer cells
- in-vitro, PC, PANC1 - in-vitro, PC, PATU-8988
EMT↓, MMPs↓, MMP2↓, MMP7↓, STAT3↓, TumCI↓, TumMeta↓, tumCV↓,
57- QC,    Quercetin inhibits angiogenesis through thrombospondin-1 upregulation to antagonize human prostate cancer PC-3 cell growth in vitro and in vivo
- vitro+vivo, PC, PC3
TSP-1↑, angioG↓, TumCMig↓, TumCI↓,
3082- RES,    Resveratrol Ameliorates the Malignant Progression of Pancreatic Cancer by Inhibiting Hypoxia-induced Pancreatic Stellate Cell Activation
- in-vitro, PC, PANC1 - in-vitro, PC, MIA PaCa-2 - in-vivo, NA, NA
VEGF↓, CXCL12↓, IL6↓, α-SMA↓, Hif1a↓, TumCI↓, EMT↓,
3035- RosA,    Rosmarinic Acid Decreases the Malignancy of Pancreatic Cancer Through Inhibiting Gli1 Signaling
- in-vitro, PC, NA - in-vivo, NA, NA
Gli1↓, TumCCA↑, TumCMig↓, TumCI↓, CDK2↓, cycE/CCNE↓, P21↑, p27↑,
962- TQ,    Thymoquinone affects hypoxia-inducible factor-1α expression in pancreatic cancer cells via HSP90 and PI3K/AKT/mTOR pathways
- in-vitro, PC, PANC1 - in-vitro, Nor, hTERT-HPNE - in-vitro, PC, AsPC-1 - in-vitro, PC, Bxpc-3
TumCMig↓, TumCI↓, Apoptosis↑, Hif1a↓, PI3k/Akt/mTOR↓, TumCCA↑, *toxicity↓, *TumCI∅, *TumCMig∅,
3130- VitC,    Effect of high-dose vitamin C on MMP2 expression and invasive ability in human pancreatic cancer cell line PANC-1
- in-vitro, PC, PANC1
MMP2↓, TumCI↓,

Showing Research Papers: 1 to 24 of 24

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 24

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GSH↓, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   ACLY↓, 1,   AMPK↑, 2,   cMyc↓, 1,   FASN↓, 1,   GAPDH↓, 1,   LDL↓, 1,   lipoGen↓, 1,   PI3K/Akt↓, 1,   PI3k/Akt/mTOR↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 2,   Apoptosis↑, 10,   BAX↑, 2,   Bcl-2↓, 3,   Casp3↑, 2,   cl‑Casp3↑, 2,   Casp7↑, 1,   Ferroptosis↑, 1,   MAPK↓, 1,   Mcl-1↓, 1,   p27↑, 1,   survivin↓, 2,   β-TRCP↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 3,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

p73↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 9,   Gli↓, 1,   Gli1↓, 4,   HH↓, 3,   p‑IGFR↓, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   Nanog↓, 1,   OCT4↓, 1,   PTCH1↓, 2,   PTCH2↓, 1,   PTEN↑, 1,   Shh↓, 2,   Smo↓, 2,   STAT3↓, 2,   Sufu↓, 1,   TOP2↓, 1,   TumCG↓, 4,  

Migration ⓘ

CXCL12↓, 1,   E-cadherin↑, 3,   GLI2↓, 1,   MMP2↓, 4,   MMP7↓, 1,   MMP9↓, 2,   MMPs↓, 1,   N-cadherin↓, 3,   NEDD9↓, 1,   Rho↓, 1,   ROCK1↓, 1,   Slug↓, 2,   p‑SMAD2↓, 2,   p‑SMAD3↓, 2,   Snail↓, 2,   TGF-β↓, 1,   TSP-1↑, 1,   TumCI↓, 24,   TumCMig↓, 14,   TumCP↓, 6,   TumMeta↓, 1,   Vim↓, 4,   Zeb1↓, 2,   α-SMA↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   HIF-1↓, 1,   Hif1a↓, 3,   VEGF↓, 3,  

Immune & Inflammatory Signaling ⓘ

CXCR4↓, 1,   IKKα↓, 1,   IL6↓, 1,   NF-kB↓, 2,  

Protein Aggregation ⓘ

BACE↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   ChemoSen↑, 1,   Dose↓, 1,   Dose↝, 1,   eff↓, 1,   eff↑, 6,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

HER2/EBBR2↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   chemoPv↑, 1,   toxicity↓, 2,   toxicity↑, 1,  
Total Targets: 105

Pathway results for Effect on Normal Cells:


Migration ⓘ

TumCI∅, 1,   TumCMig∅, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,   toxicity∅, 1,  
Total Targets: 4

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
2 Gemcitabine (Gemzar)
2 Curcumin
2 EGCG (Epigallocatechin Gallate)
2 Honokiol
2 Quercetin
1 3-bromopyruvate
1 Biochanin A
1 Atorvastatin
1 bempedoic acid
1 Brucea javanica
1 Boswellia (frankincense)
1 Chlorophyllin
1 Deguelin
1 Ginkgo biloba
1 Juglone
1 Magnolol
1 Nimbolide
1 Orlistat
1 Resveratrol
1 Rosmarinic acid
1 Thymoquinone
1 Vitamin C (Ascorbic Acid)
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:21  Cells:%  prod#:%  Target#:324  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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