F-actin Cancer Research Results

F-actin, fibrous actin: Click to Expand ⟱
Source:
Type:
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.


Scientific Papers found: Click to Expand⟱
1362- Ash,  GEM,    Synergistic Inhibition of Pancreatic Cancer Cell Growth and Migration by Gemcitabine and Withaferin A
- in-vitro, PC, PANC1 - in-vitro, PC, Hs766t
ChemoSen↑, combination treatment being the most effective
ROS↑, which were attenuated by N-acetylcysteine
Apoptosis↑,
TumCMig↓, strongest inhibition was observed when both compounds were co-administered
F-actin↓, leading to F-actin depolymerization
YMcells↓, greater reduction in cell stiffness compared to individual treatments
NF-kB↓, relative luciferase activity, which reflects NF-κB activity, was markedly elevated following treatment with GC (Figure 7). In contrast, treatment with WFA resulted in a notable decline in luciferase activity, particularly when combined with GC.

1098- BA,    Baicalein inhibits fibronectin-induced epithelial–mesenchymal transition by decreasing activation and upregulation of calpain-2
- in-vitro, Nor, MCF10 - in-vivo, NA, NA
*TumCMig↓,
*F-actin↓,
*E-cadherin↑,
*ZO-1↑,
*N-cadherin↓,
*Vim↓,
*Snail↓,
*cal2↓, baicalein inhibited calpain-2 by decreasing intracellular calcium ion levels
*Ca+2↝, Effects of baicalein on fibronectin (FN)-induced intracellular elevation of Ca2+ Returns elevated levels close to back to original levels.

5499- Ba,    Anti-cancer effects of baicalein in non-small cell lung cancer in-vitro and in-vivo
- vitro+vivo, Lung, H460 - vitro+vivo, Lung, A549
TumCP↓, Baicalein significantly decreased lung cancer proliferation in H-460 cells in a dose dependent manner.
Apoptosis↑, dose-dependent induction in apoptosis associated with decreased cellular f-actin content, an increase in nuclear condensation and an increase in mitochondrial mass potential was observed.
F-actin↓,
TumVol↓, baicalein significantly (p < 0.05) reduced tumour growth and prolonged survival.
OS↑,
12LOX↓, demonstrated reduced expression of both 12-lipoxygenase and VEGF proteins in baicalein-treated tumours, relative to untreated.
VEGF↓,
angioG↓, improves survival in-vivo, an effect that is at least partly mediated through effects on cell cycle and tumour angiogenesis.

5887- CAR,  TV,    Antitumor Effects of Carvacrol and Thymol: A Systematic Review
- Review, Var, NA
Apoptosis↑, It was attested that carvacrol and thymol induced apoptosis, cytotoxicity, cell cycle arrest, antimetastatic activity,
TumCCA↑, accumulation of cells in the G1 phase, together with a reduction of cells in the S phase, slowing cell cycle/mitosis and provoking cell death.
TumMeta↓,
TumCP↓, antiproliferative effects and inhibition of signaling pathways (MAPKs and PI3K/AKT/mTOR).
MAPK↓,
PI3K↓,
Akt↓,
mTOR↓,
eff↑, carvacrol appears to be more potent than thymol
*Inflam↓, these compounds present anti-inflammatory (Li et al., 2018; Chamanara et al., 2019) and antioxidant
*antiOx↑,
AXL↓, These effects occurred mainly through the inhibition of tyrosine kinase receptor (AXL) expression and an increase in malondialdehyde (MDA
MDA↑,
Casp3↑, caspase-3 activation and Bcl-2 inhibition
Bcl-2↓,
MMP2↓, promoted a decrease in Bcl-2, metalloproteinase-2 and -9 (MMP-2 and MMP-9), p-ERK, p-Akt, cyclin B1 levels and an increase in p-JNK, Bax levels, resulting in cell cycle arrest at the G2/M phase
MMP9↓,
p‑JNK↑,
BAX↑,
MDA↓, In respect of breast cancer, treatment with carvacrol decreases MDA-MB231 (Jamali et al., 2018; Li et al., 2021) and MCF-7 cells line viability
TRPM7↓, TRPM7 pathway is one of the suggested pharmacological mechanisms of action
MMP↓, decreased mitochondrial membrane potential, cytochrome C release, caspase activation, PARP cleavage
Cyt‑c↑,
Casp↑,
cl‑PARP↑,
ROS↑, Carvacrol also induced cytotoxicity and apoptosis (via caspase-3 and reactive oxygen species—ROS) of human oral squamous cell carcinoma (OC2 cell line)
CDK4↓, In tongue cancer (Tca-8113, SCC-25 cell lines), Dai et al. (2016) reported that carvacrol effectively inhibited cell proliferation through the negative regulation of CCND1 and CDK4 expression, and the positive regulation of p21 expression,
P21↑,
F-actin↓, A blockade of TRPM7 channels, reduced expression of MMP-2 and F-actin, was also observed, together with the inhibition of PI3K/Akt and MAPK
GSH↓, by increasing ROS, Bax, Caspase-3, -9 levels and reducing Bcl-2 and GSH levels.
*SOD↑, Moreover, carvacrol was able to increase the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione (GSH), along with a reduction of lipid peroxides and the enzymes AST, ALT, AL
*Catalase↑,
*GPx↑,
*GSR↑,
*GSH↑,
*lipid-P↓,
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
DNAdam↑, hepatocellular carcinoma induced by diethylnitrosamine (DEN), carvacrol treatment promoted DNA fragmentation
AFP↓, carvacrol showed a reduction in serum levels of alpha-fetoprotein (AFP), alpha l-fucosidase (AFU), vascular endothelial growth factor (VEGF
VEGF↓,
Weight↑, Carvacrol supplementation significantly improved the weight gain and growth rate of animals with colon cancer
*chemoP↑, reduction in oxidative stress damage (higher levels of GSH, GPx, GR, SOD and CAT), suggesting that carvacrol presents chemopreventive effects
ROS↑, In vitro, carvacrol and thymol increased the generation of reactive oxygen species in 24.63% (n = 17) of the studies, a fact that is also observed in chemotherapeutics

5885- CAR,    Inhibition of TRPM7 by carvacrol suppresses glioblastoma cell proliferation, migration and invasion
- in-vitro, GBM, U87MG - in-vitro, Nor, HEK293
TRPM7↓, investigated the effects of the TRPM7 inhibitor carvacrol on the viability, resistance to apoptosis, migration, and invasiveness of the human U87 glioblastoma cell line
tumCV↓, Carvacrol treatment reduced the viability, migration and invasion of U87 cells.
TumCMig↓, Carvacrol reduces U87 cell migration and invasion
TumCI↓, Carvacrol inhibited U87 cell migration, invasion and MMP-2 protein expression.
MMP2↓, Carvacrol also decreased MMP-2 protein expression and promoted the phosphorylation of cofilin.
toxicity↓, It's oral LD50 is 810 mg/kg in rats [26] and it is a “generally recognized as safe” food flavor additive according to the United States Food and Drug Administration.
*Inflam↓, carvacrol exhibits anti-inflammatory, antidiabetic, antinociceptive, cardioprotective, neuroprotective and anticarcinogenic properties [27]
AntiDiabetic↑,
cardioP↑,
neuroP↑,
selectivity↑, Carvacrol (CAR) blocked TRPM7 currents in HEK293 cells overexpressing TRPM7 and TRPM7-like currents in U87 cells.
Apoptosis↑, Carvacrol induces apoptosis in U87 cells
p‑Cofilin↑, Carvacrol upregulates phosphorylation of cofilin (p-cofilin) and reduces polymerization of F-actin
F-actin↓,
PI3K↓, Carvacrol suppresses PI3K/Akt and MEK/MAPK signaling pathways
Akt↓,
MEK↓,
MAPK↓,

205- MFrot,  MF,    Intermittent F-actin Perturbations by Magnetic Fields Inhibit Breast Cancer Metastasis
- vitro+vivo, BC, MDA-MB-231
OS↑, 31-46% prolonged survival
F-actin↓, decrease F-actin formation in vitro and in vivo
TumCI↓,
TumCMig↓, >4.5hrs
Rho↓,
selectivity↑, F-actin in noncancerous breast cells is much less sensitive than that in breast cancer cells, which indicate that the normal cells in our human bodies are less likely to be agitated by these magnetic fields.
TumMeta↓, Using an intermittent treatment modality, low-frequency rotating magnetic fields could significantly reduce mouse breast cancer metastasis, prolong mouse survival by 31.5 to 46.0% (P < 0.0001), and improve their overall physical condition.

1141- Myr,    Myricetin: targeting signaling networks in cancer and its implication in chemotherapy
- Review, NA, NA
*PI3K↑, apoptotic potential of myricetin is specific for affected cells. In healthy cells, it activates PI3K/Akt signaling and inhibits ERK/JNK pathway to induce cytoprotective influence
*Akt↑,
p‑Akt↓,
SIRT3↑,
p‑ERK↓,
p38↓,
VEGF↓,
MEK↓, MEK1
MKK4↓,
MMP9↓,
Raf↓,
F-actin↓,
MMP2↓,
COX2↓,
BMP2↓,
cycD1/CCND1↓,
Bax:Bcl2↑,
EMT↓,
EGFR↓,
TumAuto↑,

2952- PL,    Piperlongumine suppresses bladder cancer invasion via inhibiting epithelial mesenchymal transition and F-actin reorganization
- in-vitro, Bladder, T24/HTB-9 - in-vivo, Bladder, NA
TumCP↓, PL significantly suppressed bladder cancer cell proliferation, the transition of G2/M phase to next phase, migration/invasion in vitro and bladder cancer growth/development in vivo
TumCCA↑,
TumCMig↓,
TumCI↓,
ROS↑, PL markedly elevated reactive oxygen species (ROS)
Slug↓, PL inhibited epithelial mesenchymal transition with profoundly decreased level of Slug, β-catenin, ZEB1 and N-Cadherin.
β-catenin/ZEB1↓,
Zeb1↓,
N-cadherin↓,
F-actin↓, decreased F-actin intensity in bladder cancer cells
GSH↓, Consistently, intracellular glutathione (GSH) levels were significantly reduced in T24 cells at 3 h of PL treatment
EMT↓, PL inhibited epithelial mesenchymal transition
CLDN1↓, The decline of Claudin-1 and ZO-1 upon PL treatment
ZO-1↓,


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 2,   MDA↓, 1,   MDA↑, 1,   ROS↑, 4,   SIRT3↑, 1,  

Mitochondria & Bioenergetics ⓘ

MEK↓, 2,   MKK4↓, 1,   MMP↓, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 1,   Apoptosis↑, 4,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   BMP2↓, 1,   Casp↑, 1,   Casp3↑, 1,   Cyt‑c↑, 1,   p‑JNK↑, 1,   MAPK↓, 2,   p38↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,   YMcells↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   p‑ERK↓, 1,   mTOR↓, 1,   PI3K↓, 2,   TRPM7↓, 2,  

Migration ⓘ

AXL↓, 1,   CLDN1↓, 1,   p‑Cofilin↑, 1,   F-actin↓, 7,   MMP2↓, 3,   MMP9↓, 2,   N-cadherin↓, 1,   Rho↓, 1,   Slug↓, 1,   TumCI↓, 3,   TumCMig↓, 4,   TumCP↓, 3,   TumMeta↓, 2,   Zeb1↓, 1,   ZO-1↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   VEGF↓, 3,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

AFP↓, 1,   EGFR↓, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 1,   neuroP↑, 1,   OS↑, 2,   toxicity↓, 1,   TumVol↓, 1,   Weight↑, 1,  
Total Targets: 70

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSR↑, 1,   lipid-P↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   LDH↓, 1,  

Cell Death ⓘ

Akt↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↑, 1,  

Migration ⓘ

Ca+2↝, 1,   cal2↓, 1,   E-cadherin↑, 1,   F-actin↓, 1,   N-cadherin↓, 1,   Snail↓, 1,   TumCMig↓, 1,   Vim↓, 1,   ZO-1↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,  
Total Targets: 26

Scientific Paper Hit Count for: F-actin, fibrous actin
2 Carvacrol
1 Ashwagandha(Withaferin A)
1 Gemcitabine (Gemzar)
1 Baicalin
1 Baicalein
1 Thymol-Thymus vulgaris
1 Magnetic Field Rotating
1 Magnetic Fields
1 Myricetin
1 Piperlongumine
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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