fascin Cancer Research Results

fascin, fascin: Click to Expand ⟱
Source:
Type: protein
Fascin is a protein that plays a crucial role in the regulation of cell adhesion, migration, and signaling. In the context of cancer, fascin has been found to be overexpressed in various types of tumors, including breast, lung, colon, and esophageal cancers.
Scientific Papers found: Click to Expand⟱
6462- 1,8-Cin,    Modes of Action of 1,8-Cineol in Infections and Inflammation
- Review, Var, NA - Review, AD, NA
*BioAv↑, become increasingly clear in the recent years that 1,8-Cineol spreads almost everywhere in the human body after its oral administration, from the gut to the blood to the brain.
*BBB↑,
*AntiViral↑, anti-viral effects have been observed to include numerous bacteria and fungi species.
*Bacteria↓,
*AntiFungal↑,
*Inflam↓, central mode of action of 1,8-Cineol is the inhibition of pro-inflammatory cytokine expression
*BioAv↑, 1,8-Cineol was detectable in nasal tissue samples after its oral administration for 14 days, which indicates the systemic distribution of 1,8-Cineol via the gut and the blood stream
*MUC2↓, significantly reduced expression levels of the mucin genes MUC2 and MUC19 in close association with a significantly attenuated activity of transcription factor NF-κB
*MUC19↓,
*NF-kB↓, reduced the expression levels of transcriptional activator nuclear factor (NF)-kB p65 and expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in lung tissues
*ICAM-1↓,
*VCAM-1↓,
DNAdam↑, colon cancer cells on the potential genotoxicity of 1,8-Cineol revealed a concentration-dependent increase in oxidative DNA damage, whereas it did not affect the cell viability due to DNA repair mechanisms
*lipid-P↓, suppressing the expression of lipid mediators and prostaglandin D2
*PGE2↓,
*IL4↓, decreased expression levels of different inflammatory cytokines such as interleukin (IL)-4, IL-6 and granulocyte macrophage colony stimulating factor (GM-CSF) in bronchial epithelial cells
*IL6↓,
*IL1β↓, 1,8-Cineol-containing leaf extracts significantly suppressed the expression of pro-inflammatory cytokines IL-1β and IL-6 [
*IL6↓,
eff↑, 1,8-Cineol in combination with ellagic acid has been shown to downregulate different cytokines such as transforming growth factor beta-1 (TGF-β1), Fascin-1 (FSCN1), vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) in p
TGF-β↓,
fascin↓,
VEGF↓,
MMP9↓,
*MAPK↓, 1,8-Cineol was shown to suppress the activation of the MAPK/ERK
*ERK↓,
JNK↓, decreased activities of transcription factor NFκB and the JNK (c-Jun N-terminal kinase)/AP-1 (activator protein-1) pathway in the human cancer cell lines U373 and HeLa in response to 1,8-Cineol, the active ingredient of the drug Soledum
Wnt↓, 1,8-Cineol acts as an inhibitor of the Wnt/β-catenin pathway in head and neck squamous cell carcinoma (HNSCC).
β-catenin/ZEB1↓,
GSK‐3β↑, decreased inhibition of glycogen synthase kinase 3 (GSK-3) and reduced levels of WNT11
*neuroP↑, 1,8-Cineol has been shown to have neuroprotective activity.
*GSK‐3β↓, decreased activity of GSK-3 in response to 1,8-Cineol could ameliorate advanced glycation end products,
*AGEs↓,
*BBB↑, eucalyptol reveals an opening effect on the blood–brain barrier
*NLRP3↓, controls inflammation by suppressing the NOD-like receptor pyrin domain-containing 3 (NLRP3) activation

469- CUR,    The inhibitory effect of curcumin via fascin suppression through JAK/STAT3 pathway on metastasis and recurrence of ovary cancer cells
- in-vitro, Ovarian, SKOV3
fascin↓,
STAT3↓,
JAK↓,

7631- Ins,  IP6,    Broad Spectrum Anticancer Activity of Myo-Inositol and Inositol Hexakisphosphate
- Review, Var, NA
other↑, Deregulated inositol metabolism has been recorded in a number of diseases, including cancer, where inositol modulates different critical pathways.
p‑pRB↓, Inositols inhibit pRB phosphorylation, fostering the pRB/E2F complexes formation and blocking progression along the cell cycle.
TumCCA↑,
PI3K↓, Inositols reduce PI3K levels, thus counteracting the activation of the PKC/RAS/ERK pathway downstream of PI3K activation.
Akt↓, Akt activation is severely impaired upon inositol addition
ERK↓, Downregulation of both Akt and ERK leads consequently to NF-kB inhibition and reduced expression of inflammatory markers (COX-2 and PGE2).
NF-kB↓,
COX2/PTGS2↓,
PGE2↓,
PSEN1/PS1↓, Remarkably, inositol-induced downregulation of presenilin-1 interferes with the epithelial-mesenchymal transition and reduces Wnt-activation, β-catenin translocation, Notch-1, N-cadherin, and SNAI1 release.
EMT↓,
Wnt↓,
β-catenin/ZEB1↓,
NOTCH1↓,
N-cadherin↓,
Snail↓,
E-cadherin↑, upregulating Focal Adhesion Kinase and E-cadherin and decreasing Fascin and Cofilin, two main components of pseudopodia, leading hence to invasiveness impairment.
fascin↓,
Cofilin↓,
MMPs↓, inositol-induced inhibition on metalloproteinases and ROCK1/2 release
ROCK1↓,
Dose↝, A mixed western diet provides the human adult with approximately 1 g of total inositol per day. it may be surmised that in western countries low-vegetable consumers may suffer from a relative deficiency of myo-Ins
other↝, InsP6 is often referred to as an antinutrient [20] responsible for iron deficiencies mostly in underdeveloped countries, it should be emphasized that InsP6 displays its antinutritional effects only when the diet is already deprived of trace elements
selectivity↑, specific for cancer cells, given that both InsP6 and myo-Ins did not promote apoptosis in normal cells.
*ROS↓, Myo-Ins counteracts oxidative damage in fish exposed to environmental stresses [114] and significantly inhibits systemic markers of oxidative stress in gynecological patients
*lipid-P↓, thus preventing formation of ADP-iron-oxygen complexes that trigger lipid peroxidation
ROS↑, antioxidant property of inositol is strictly context-dependent as, under specific conditions, both myo-Ins and InsP6 may increase free radical production
NK cell↑, inositol hexakisphosphate and myo-Ins enhance NK activity in mice treated with 1,2-dimethylhydrazine (DMH),
Imm↑, enhancement of immune function
TNF-α↓, InsP6 also modulates the transcription genes for TNF by decreasing it and its receptors in colon cancer cells
ChemoSen↑, inositol hexakisphosphate may potentiate the anticancer effects of conventional chemotherapy in preventing the successful development of cancer implants
Dose↑, Mild side effects (mostly represented by nausea or diarrhea) are reported in a small fraction of subjects, only for doses up to 12 g/day
toxicity↓,
QoL↑, where InsP6 plus myo-Ins treatment is associated with appreciable reduction in tumor burden and improved quality of life
chemoP↑, , if inositols were added along with conventional chemotherapy, colon cancer patients experienced significantly less side effects than controls, as reported in a pilot study
OS↑, Furthermore, prolonged survival and better quality of life have been obtained in some anecdotal cases of breast and lung cancer patients treated with InsP6 and myo-Ins
Dose↝, A study enrolling 26 smokers showed that myo-Ins in a daily dose up to 18 g/p.o. is safe and well tolerated, while inducing a significant regression of individual pulmonary dysplastic lesions
Insulin↓, downregulation of insulin levels, improved glucose utilization through the oxidative cycle, and inhibition of lipogenesis).
glucose↝,
lipoGen↓,
eff↑, There is a widespread consensus suggesting that InsP6 and myo-Ins act synergistically when added in association.


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

PSEN1/PS1↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

Insulin↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

glucose↝, 1,   lipoGen↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   JNK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,   other↝, 1,   p‑pRB↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 1,   ERK↓, 1,   GSK‐3β↑, 1,   NOTCH1↓, 1,   PI3K↓, 1,   STAT3↓, 1,   Wnt↓, 2,  

Migration(tgid=13) ⓘ

Cofilin↓, 1,   E-cadherin↑, 1,   fascin↓, 3,   MMP9↓, 1,   MMPs↓, 1,   N-cadherin↓, 1,   ROCK1↓, 1,   Snail↓, 1,   TGF-β↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   Imm↑, 1,   JAK↓, 1,   NF-kB↓, 1,   NK cell↑, 1,   PGE2↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose↑, 1,   Dose↝, 2,   eff↑, 2,   selectivity↑, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1,   OS↑, 1,   QoL↑, 1,   toxicity↓, 1,  
Total Targets: 46

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

lipid-P↓, 2,   ROS↓, 1,  

Cell Death(tgid=5) ⓘ

MAPK↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↓, 1,   GSK‐3β↓, 1,  

Migration(tgid=13) ⓘ

VCAM-1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

ICAM-1↓, 1,   IL1β↓, 1,   IL4↓, 1,   IL6↓, 2,   Inflam↓, 1,   MUC2↓, 1,   NF-kB↓, 1,   PGE2↓, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 2,   MUC19↓, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   AntiViral↑, 1,   Bacteria↓, 1,  
Total Targets: 24

Scientific Paper Hit Count for: fascin, fascin
1 1,8-Cineole
1 Curcumin
1 Inositol
1 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
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

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