F-actin Cancer Research Results
F-actin, fibrous actin: Click to Expand ⟱
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A fibrous actin polymerized in the form of a double helix that is produced in the presence of a metal cation (as of calcium) and ATP.
Dynamic rearrangements of the F-actin cytoskeleton are a hallmark of tumor metastasis.
F-actin plays a significant role in the progression and prognosis of various cancers. Its expression and dynamics are often linked to increased invasiveness, metastatic potential, and treatment resistance. In many cancer types, high levels of F-actin correlate with poor prognosis and aggressive disease.
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Scientific Papers found: Click to Expand⟱
*eff↑, Pulsed electromagnetic fields (PEMFs) are currently used as a safe and non-invasive treatment to enhance bone healing and to provide joint protection.
*COL2A1↑, exposure to PEMFs induced increased collagen type II (Col2) expression and glycosaminoglycan (GAG) content
*SOX9↑, PEMFs significantly increased the expression of chondrogenic genes (SOX9, collagen type II, and aggrecan) and the deposition of cartilaginous matrix (sulphated GAG)
*Ca+2↑, Intracellular Ca2+ increase
*FAK↑, FAK activation
*F-actin↑, increased F-actin network formation
*Inflam↓, anti-inflammatory effect of PEMFs exposure has been extensively described above
*other↑, PEMFs exert a strong anti-inflammatory effect protecting cartilage tissue from the catabolic activity of pro-inflammatory cytokines.
*Diff↑, commonly recognized that PEMFs exposure induces osteogenic differentiation of MSCs
*BMD↑, Emerging evidence shows that PEMFs stimulation represents a safe non-invasive approach to favor bone repair and optimize bone tissue engineering
Glycolysis↓, We find that VD3 treatment significantly down-regulates glycolytic enzymes and genes and decreases glucose uptake - for both lowly metastatic MCF-7 and highly metastatic MDA-MB-231 (MB231) breast cancer cells.
tumCV↓, VD3 also significantly decreases cell viability by inducing apoptosis
Apoptosis↑,
mTOR↓, consistent with decreased expression of mammalian target of rapamycin (mTOR),
AMPK↑, increases 5' adenosine monophosphate-activated protein kinase (AMPK) activation
EMT↓, presumably a consequence of reversal of the epithelial to mesenchymal transition
E-cadherin↑, increased E-cadherin, and F-actin, and reduced vimentin expression
F-actin↑,
Vim↓,
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:
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, Glycolysis↓, 1,
Cell Death ⓘ
Apoptosis↑, 1,
Transcription & Epigenetics ⓘ
tumCV↓, 1,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, mTOR↓, 1,
Migration ⓘ
E-cadherin↑, 1, F-actin↑, 1, Vim↓, 1,
Total Targets: 9
Pathway results for Effect on Normal Cells:
Kinase & Signal Transduction ⓘ
SOX9↑, 1,
Transcription & Epigenetics ⓘ
other↑, 1,
Proliferation, Differentiation & Cell State ⓘ
Diff↑, 1,
Migration ⓘ
Ca+2↑, 1, COL2A1↑, 1, F-actin↑, 1, FAK↑, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1,
Drug Metabolism & Resistance ⓘ
eff↑, 1,
Clinical Biomarkers ⓘ
BMD↑, 1,
Total Targets: 10
Scientific Paper Hit Count for: F-actin, fibrous actin
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#:565 State#:% Dir#:2
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