FGF Cancer Research Results

FGF, Fibroblast growth factors: Click to Expand ⟱
Source:
Type:
Fibroblast growth factors (FGFs) have diverse functions in the regulation of cell proliferation and differentiation in development, tissue maintenance, wound repair, and angiogenesis.

FGFs play a significant role in cancer biology, influencing processes such as cell proliferation, survival, and angiogenesis. Their expression is often associated with poor prognosis and increased tumor aggressiveness across various cancer types. Targeting FGF signaling pathways is being explored as a potential therapeutic strategy in cancer treatment.


Scientific Papers found: Click to Expand⟱
2711- BBR,    Berberine inhibits the progression of breast cancer by regulating METTL3-mediated m6A modification of FGF7 mRNA
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
TumCP↓, BBR treatment hindered breast cancer cell proliferation, invasion, migration, and induced apoptosis
TumCI↓,
TumCMig↓,
Apoptosis↑,
FGF↓, FGF7 expression was upregulated in breast cancer tissues, while its level was reduced in BBR-treated tumor cells
IGFBP3↑, IGF2BP3 recognized the m6A modification of FGF7 mRNA and enhanced its expression

6542- BSB,    Health Benefits, Pharmacological Effects, Molecular Mechanisms, and Therapeutic Potential of α-Bisabolol
- Review, Var, NA - Review, Park, NA - Review, AD, NA
AntiCan↑, Numerous experimental studies demonstrated pharmacological properties of α-Bisabolol including anticancer, antinociceptive, neuroprotective, cardioprotective, and antimicrobial.
*neuroP↑,
*cardioP↑,
*AntiBio↑,
*BioAv↑, Given the polypharmacological effects and pleiotropic properties, along with favorable pharmacokinetics, and dietary availability and safety, α-Bisabolol can be used as a dietary agent, nutraceutical or phytopharmaceutical agent or as an adjuvant wit
*toxicity↓,
*BioAv↑, integrated in many cosmetic formulations due to its skin soothing effects, well documented dermal absorption
*motorD↑, improvement in locomotor activity, a reduction in the expression of thiol and a reinstate of the activity of mitochondrial complex-I.
*SOD↑, α-Bisabolol also increased the mRNA level of antioxidants proteins such as superoxide dismutase (SOD), catalase (CAT), and the keap1 gene product.
*Catalase↑,
*Keap1↑,
*MDA↓, α-Bisabolol attenuated oxidative insult by reducing malondialdehyde (MDA), restoring depleted glutathione (GSH) and improving SOD and CAT activity.
*GSH↑,
*IL1β↓, attenuated neuroinflammation by reducing glial cells activation and subsequent release of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and mediators (iNOS and COX-2).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2↓,
*lipid-P↓, α-Bisabolol restored mitochondrial function by preventing mitochondrial lipid peroxidation, cytochrome-C release and most importantly preserving Complex-I activity
*Cyt‑c↓,
*ROS↓, The study concluded that α-Bisabolol safeguarded against the induced upsurge of ROS and nitrite.
*MMP↑, α-Bisabolol treatment also restored mitochondrial membrane potential (MMP) validating its antioxidant effect.
*antiOx↑,
*AChE↓, showed a significant reduction in AChE activity and an ability to avert Ach depletion.
*Apoptosis↓, α-Bisabolol protected cells from Aβ triggered apoptosis by reducing Bax and Caspase-3 and increasing Bcl-2 activity.
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BACE↓, α-Bisabolol inhibitory activity on BACE1 and found a decrease in BACE1 activity following α-Bisabolol treatment
*BChE↓, AChE, BuChE, β-secretase actions were decreased significantly in cells pretreated with α-Bisabolol
*eff↑, The compound clearly illustrated a potent anti-AchE activity of 95.869% similar to the activity of donepezil, a standard drug. I
*Aβ↓, The compound also disaggregated Aβ25–35 peptide and protected against its induced toxicity by increasing neuro2a cells viability [
*ATP↑, figure 2
RadioS↑, α-Bisabolol and Anticancer Effects, figure 3
Cyt‑c↑,
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↑,
PARP↑,
BAX↑,
BID↑,
NF-kB↑,
Fas↑,
EGFR↑,
TIMP2↑,
XIAP↓,
COX2↓,
Bak↓,
Bcl-2↓,
P53↑, The expression of p53 (a transcription factors whose products might lead to apoptosis), NF-κB and Fas was increased following α-Bisabolol treatment, indicating their function in mediating α-Bisabolol-induced apoptosis in the cancer cell line.
HER2/EBBR2↓,
FGF↓,
CEA↓,
Akt↓,
TumCCA↑, α-Bisabolol suppresses the cellular proliferation at G2/M cell cycle phase.
*Imm↑, reported that α-Bisabolol boosted the immunity response by T-cell subsets (CD4 and CD8) supplementation in treated mice.
*CD4+↑,
*CD8+↑,
*BBB↑, ↑ BBB penetration
*Pain↓, α-Bisabolol based mouthwash to that of chlorhexidine in reducing pain during brushing
*cardioP↑, α-Bisabolol and Cardioprotection, figure 5
*TBARS↓, rats co-treated with α-Bisabolol showed reduced LOOH and TBARS and increased SOD, CAT and GSH.
*SOD↑,
*Catalase↑,
*GSH↑,
*AntiBio↑, α-Bisabolol demonstrated an antibacterial effect against Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa as well as a synergism against S. aureus, when combined with the antibiotic norfloxacin and against E. coli when combined with
*AntiFungal↑, ↓ fungal growth
*GastroP↑, α-Bisabolol and Gastroprotection. oral administration of α-Bisabolol was realized to attenuate gastric damage and to provide cytoprotection in stomach.
*RenoP↑, The nephroprotective effects of α-Bisabolol and the underlying mechanisms are summarized in Table 10.
*creat↓, ↓ creatinine, urea, uric acid
*uricA↓,
*Inflam↓, Anti-Inflammatory Effects of α-Bisabolol
*iNOS↓, ↓ iNOS, COX-2, TNF-α, p65 PGE2, nitrite, IL-6, ↓ MMP13
*COX2↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,

13- CUR,    Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action
- Review, BC, NA
P53↑, upregulated other targets including p53, death receptor (DR-5), JN-kinase, Nrf-2, and peroxisome proliferator-activated receptor γ (PPARγ) factors
DR5↑,
JNK↑,
NRF2↑,
PPARγ↑,
HER2/EBBR2↓, (Her-2, IR, ER-a, and Fas receptor)
IR↓,
ER(estro)↓,
Fas↑,
PDGF↓, (PDGF, TGF, FGF, and EGF)
TGF-β↓,
FGF↓,
EGFR↓,
JAK↓,
PAK↓,
MAPK↓,
ATPase↓, (ATPase, COX-2, and matrix metalloproteinase enzyme [MMP])
COX2↓,
MMPs↓,
IL1↓, inflammatory cytokines (IL-1, IL-2, IL-5, IL-6, IL-8, IL-12, and IL-18)
IL2↓,
IL5↓,
IL6↓,
IL8↓,
IL12↓,
IL18↓,
NF-kB↓,
NOTCH1↓,
STAT1↓,
STAT4↓,
STAT5↓,
STAT3↓,

26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
BAD↓,
cl‑PARP↑,
Casp7↑,
IκB↓,
Ki-67↓,
VEGF↓,
EGFR↓,
FGF↓,
TGF-β↓,
TNF-α↓,
SCF↓,
Bax:Bcl2↑,
NF-kB↓,
chemoP↑, This study provides a novel regimen to enhance the therapeutic effect of Doc in a less-toxic manner and reduce its risk of side effects in treatment of CRPC.
ChemoSen↑, GT and Q with LD Doc significantly enhanced the potency of Doc 2-fold and reduced tumor growth by 62 % compared to LD Doc in 7-weeks intervention.
TumVol↓,

1656- FA,    Ferulic Acid: A Natural Phenol That Inhibits Neoplastic Events through Modulation of Oncogenic Signaling
- Review, Var, NA
tyrosinase↓,
CK2↓,
TumCP↓,
TumCMig↓,
FGF↓,
FGFR1↓,
PI3K↓,
Akt↓,
VEGF↓,
FGFR1↓,
FGFR2↓,
PDGF↓,
ALAT↓,
AST↓,
TumCCA↑, G0/G1 phase arrest
CDK2↓,
CDK4↓,
CDK6↓,
BAX↓,
Bcl-2↓,
MMP2↓,
MMP9↓,
P53↑,
PARP↑,
PUMA↑,
NOXA↑,
Casp3↑,
Casp9↑,
TIMP1↑,
lipid-P↑,
mtDam↑,
EMT↓,
Vim↓,
E-cadherin↓,
p‑STAT3↓,
COX2↓,
CDC25↓,
RadioS↑,
ROS↑,
DNAdam↑,
γH2AX↑,
PTEN↑,
LC3II↓,
Beclin-1↓,
SOD↓,
Catalase↓,
GPx↓,
Fas↑,
*BioAv↓, ferulic acid stability and limited solubility in aqueous media continue to be key obstacles to its bioavailability, preclinical efficacy, and clinical use.
cMyc↓,
Beclin-1↑, ferulic acid by elevating the levels of the apoptosis and autophagy biomarkers, including beclin-1, Light chain (LC3-I/LC3-II), PTEN-induced putative kinase 1 (PINK-1), and Parkin
LC3‑Ⅱ/LC3‑Ⅰ↓,

3369- QC,    Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects
- Review, Pca, NA
FAK↓, Quercetin can inhibit HGF-induced melanoma cell migration by inhibiting the activation of c-Met and its downstream Gabl, FAK and PAK [84]
TumCCA↑, stimulation of cell cycle arrest at the G1 stage
p‑pRB↓, mediated through regulation of p21 CDK inhibitor and suppression of pRb phosphorylation resulting in E2F1 sequestering.
CDK2↑, low dose of quercetin has brought minor DNA injury and Chk2 induction
CycB/CCNB1↓, quercetin has a role in the reduction of cyclin B1 and CDK1 levels,
CDK1↓,
EMT↓, quercetin suppresses epithelial to mesenchymal transition (EMT) and cell proliferation through modulation of Sonic Hedgehog signaling pathway
PI3K↓, quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
MAPK↓,
Wnt↓,
ROS↑, colorectal cancer, quercetin has been shown to suppress carcinogenesis through various mechanisms including affecting cell proliferation, production of reactive oxygen species and expression of miR-21
miR-21↑,
Akt↓, Figure 1 anti-cancer mechanisms
NF-kB↓,
FasL↑,
Bak↑,
BAX↑,
Bcl-2↓,
Casp3↓,
Casp9↑,
P53↑,
p38↑,
MAPK↑,
Cyt‑c↑,
PARP↓,
CHOP↑,
ROS↓,
LDH↑,
GRP78/BiP↑,
ERK↑,
MDA↓,
SOD↑,
GSH↑,
NRF2↑,
VEGF↓,
PDGF↓,
EGF↓,
FGF↓,
TNF-α↓,
TGF-β↓,
VEGFR2↓,
EGFR↓,
FGFR1↓,
mTOR↓,
cMyc↓,
MMPs↓,
LC3B-II↑,
Beclin-1↑,
IL1β↓,
CRP↓,
IL10↓,
COX2↓,
IL6↓,
TLR4↓,
Shh↓,
HER2/EBBR2↓,
NOTCH↓,
DR5↑, quercetin has enhanced DR5 expression in prostate cancer cells
HSP70/HSPA5↓, Quercetin has also suppressed the upsurge of hsp70 expression in prostate cancer cells following heat treatment and enhanced the quantity of subG1 cells
CSCs↓, Quercetin could also suppress cancer stem cell attributes and metastatic aptitude of isolated prostate cancer cells through modulating JNK signaling pathway
angioG↓, Quercetin inhibits angiogenesis-mediated of human prostate cancer cells through negatively modulating angiogenic factors (TGF-β, VEGF, PDGF, EGF, bFGF, Ang-1, Ang-2, MMP-2, and MMP-9)
MMP2↓,
MMP9↓,
IGFBP3↑, Quercetin via increasing the level of IGFBP-3 could induce apoptosis in PC-3 cells
uPA↓, Quercetin through decreasing uPA and uPAR expression and suppressing cell survival protein and Ras/Raf signaling molecules could decrease prostate cancer progression
uPAR↓,
RAS↓,
Raf↓,
TSP-1↑, Quercetin through TSP-1 enhancement could effectively inhibit angiogenesis


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   GPx↓, 1,   GSH↑, 1,   lipid-P↑, 1,   MDA↓, 1,   NRF2↑, 2,   ROS↓, 1,   ROS↑, 2,   SOD↓, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↓, 1,   EGF↓, 1,   FGFR1↓, 3,   mtDam↑, 1,   Raf↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   cMyc↓, 2,   IR↓, 1,   LDH↑, 1,   PPARγ↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Apoptosis↑, 2,   BAD↓, 1,   Bak↓, 1,   Bak↑, 1,   BAX↓, 1,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   BID↑, 1,   Casp3↓, 1,   Casp3↑, 2,   Casp7↑, 1,   Casp8↑, 1,   Casp9↑, 3,   CK2↓, 1,   Cyt‑c↑, 2,   DR5↑, 2,   Fas↑, 3,   FasL↑, 1,   JNK↑, 1,   MAPK↓, 2,   MAPK↑, 1,   NOXA↑, 1,   p38↑, 1,   PUMA↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 3,   PAK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

miR-21↑, 1,   p‑pRB↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↑, 1,   GRP78/BiP↑, 1,   HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,   Beclin-1↑, 2,   LC3‑Ⅱ/LC3‑Ⅰ↓, 1,   LC3B-II↑, 1,   LC3II↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   P53↑, 4,   PARP↓, 1,   PARP↑, 2,   cl‑PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK2↑, 1,   CDK4↓, 1,   CycB/CCNB1↓, 1,   TumCCA↑, 3,  

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

CSCs↓, 1,   EMT↓, 2,   ERK↑, 1,   FGF↓, 6,   FGFR2↓, 1,   IGFBP3↑, 2,   mTOR↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   PI3K↓, 2,   PTEN↑, 1,   RAS↓, 1,   SCF↓, 1,   Shh↓, 1,   STAT1↓, 1,   STAT3↓, 1,   p‑STAT3↓, 1,   STAT4↓, 1,   STAT5↓, 1,   tyrosinase↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

ATPase↓, 1,   CEA↓, 1,   E-cadherin↓, 1,   FAK↓, 1,   Ki-67↓, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 2,   PDGF↓, 3,   TGF-β↓, 3,   TIMP1↑, 1,   TIMP2↑, 1,   TSP-1↑, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 2,   uPA↓, 1,   uPAR↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   EGFR↓, 3,   EGFR↑, 1,   VEGF↓, 3,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 4,   CRP↓, 1,   IL1↓, 1,   IL10↓, 1,   IL12↓, 1,   IL18↓, 1,   IL1β↓, 1,   IL2↓, 1,   IL5↓, 1,   IL6↓, 2,   IL8↓, 1,   IκB↓, 1,   JAK↓, 1,   NF-kB↓, 3,   NF-kB↑, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,   ER(estro)↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   RadioS↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   CEA↓, 1,   CRP↓, 1,   EGFR↓, 3,   EGFR↑, 1,   HER2/EBBR2↓, 3,   IL6↓, 2,   Ki-67↓, 1,   LDH↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   chemoP↑, 1,   TumVol↓, 1,  
Total Targets: 150

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 2,   GSH↑, 2,   Keap1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   ROS↓, 1,   SOD↑, 2,   TBARS↓, 1,   uricA↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   MMP↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   BAX↓, 1,   Bcl-2↑, 1,   Casp3↓, 1,   Cyt‑c↓, 1,   iNOS↓, 2,  

Migration(tgid=13) ⓘ

MMP13↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GastroP↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2↓, 2,   IL1β↓, 1,   IL6↓, 1,   IL6↑, 1,   Imm↑, 1,   Inflam↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   BChE↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 2,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

creat↓, 1,   IL6↓, 1,   IL6↑, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 2,   motorD↑, 1,   neuroP↑, 1,   Pain↓, 1,   RenoP↑, 1,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   CD8+↑, 1,  
Total Targets: 48

Scientific Paper Hit Count for: FGF, Fibroblast growth factors
2 Quercetin
1 Berberine
1 α-Bisabolol / Chamomile oil
1 Curcumin
1 EGCG (Epigallocatechin Gallate)
1 Docetaxel
1 Ferulic acid
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#:362  State#:%  Dir#:1
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