Cofilin Cancer Research Results

Cofilin, Cofilin: Click to Expand ⟱
Source:
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.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
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↓, annexin II↓, Cofilin↓, Rho↑, APAF1↑, TRAF2↑, Apoptosis↑, PI3K↓, Akt↓,
8076- KAE,    Kaempferol suppresses prostate cancer metastasis and tumor angiogenesis via disrupting the LIMK1/Cofilin pathway
- in-vivo, Pca, NA
AntiTum↑, TumCP↓, TumCCA↑, VEGF↓, CDK4↓, CDK6↓, LIMK1↓, Cofilin↓, angioG↓,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

LIMK1↓, 1,   TRAF2↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   TumCCA↑, 1,  

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

PI3K↓, 1,  

Migration(tgid=13) ⓘ

annexin II↓, 1,   Cofilin↓, 2,   Rho↑, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,  
Total Targets: 17

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Cofilin, Cofilin
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:22  Cells:%  prod#:%  Target#:1013  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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