Cofilin Cancer Research Results

Cofilin, Cofilin: Click to Expand ⟱
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Type:
Cofilin is an actin-binding protein that plays a central role in regulating actin dynamics and cytoskeletal remodeling. Its activity is essential for various cellular functions, including migration, invasion, and cell division.

High levels of active cofilin have been associated with increased invasiveness and metastatic potential in several tumor types, often correlating with a poorer prognosis. Assessing cofilin activity (for example, via levels of phosphorylated vs. non-phosphorylated protein) might provide insights into the metastatic potential of a tumor.
Scientific Papers found: Click to Expand⟱
7628- Ins,    Proteomic Analysis of Anticancer Effect of Myo-inositol in Human Prostate Cancer (DU-145) Cell Line
- in-vitro, Pca, DU145
tumCV↓, Myo-inositol significantly reduced DU-145 cell viability with an IC50 of 0.06 mg/ml (p<0.05).
annexin II↓, with suppression of proteins like Annexin A2 and Cofilin-1-A in controls, and upregulation of proteins such as Rho GTPase-activating protein, Apoptotic protease-activating factor 1 (APAF1), and TNF receptor-associated factor 2 (TRAF2)
Cofilin↓,
Rho↑,
APAF1↑,
TRAF2↑,
Apoptosis↑, Myo-inositol and its derivatives limit cell growth and trigger apoptosis in breast, colon, and prostate cancer cell lines via disturbed pathways like the PI3K/Akt pathway.
PI3K↓,
Akt↓,

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.

1133- SM,    Salvianolic Acid A, a Component of Salvia miltiorrhiza, Attenuates Endothelial-Mesenchymal Transition of HPAECs Induced by Hypoxia
- in-vitro, Nor, HPAECs
*ROS↓,
*p‑Smad1↑,
*p‑SMAD5↑,
*SMAD2↓,
*SMAD3↓,
*p‑ERK↓,
*p‑Cofilin↓,


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,   TRAF2↑, 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↓, 2,   APAF1↑, 1,   Apoptosis↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

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

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

EMT↓, 1,   ERK↓, 1,   NOTCH1↓, 1,   PI3K↓, 2,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

annexin II↓, 1,   Cofilin↓, 2,   E-cadherin↑, 1,   fascin↓, 1,   MMPs↓, 1,   N-cadherin↓, 1,   Rho↑, 1,   ROCK1↓, 1,   Snail↓, 1,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

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

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1,   OS↑, 1,   QoL↑, 1,   toxicity↓, 1,  
Total Targets: 44

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

lipid-P↓, 1,   ROS↓, 2,  

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

p‑ERK↓, 1,  

Migration(tgid=13) ⓘ

p‑Cofilin↓, 1,   p‑Smad1↑, 1,   SMAD2↓, 1,   SMAD3↓, 1,   p‑SMAD5↑, 1,  
Total Targets: 8

Scientific Paper Hit Count for: Cofilin, Cofilin
2 Inositol
1 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
1 Salvia miltiorrhiza
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#:1013  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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