TumPF Cancer Research Results

TumPF, Tumor-promoting fibroblasts: Click to Expand ⟱
Source: HalifaxProj(deactivate)
Type:
Tumor-promoting fibroblasts, often referred to as cancer-associated fibroblasts (CAFs), play a significant role in the tumor microenvironment and contribute to cancer progression.
CAFs are derived from various sources, including resident fibroblasts, mesenchymal stem cells, and even epithelial cells through a process called epithelial-to-mesenchymal transition (EMT). They exhibit distinct characteristics compared to normal fibroblasts, including altered gene expression and increased secretion of growth factors and cytokines.
Scientific Papers found: Click to Expand⟱
7185- CHA,    Chaetocin-induced ROS-mediated apoptosis involves ATM–YAP1 axis and JNK-dependent inhibition of glucose metabolism
- vitro+vivo, GBM, A172 - in-vitro, GBM, T98G - in-vitro, GBM, U87MG
HMTs↓, Chaetocin, a histone methyltransferase inhibitor, is known to induce ROS generation.
ROS↑,
p‑ATM↑, Chaetocin-treated tumors exhibited heightened ROS, pATM, YAP1 and pJNK levels
YAP/TEAD↑, An increase in YAP1 level and decrease in YAP1 phosphorylation was observed upon Chaetocin treatment
p‑JNK↑,
TumPF↓, Chaetocin inhibits glioma cell proliferation
SUV39H↓, Chaetocin, an inhibitor of lysine-specific histone methyltransferase SUV39H1
TrxR↓, Chaetocin reduces thioredoxin reductase activity in a dose-dependent manner.
Casp3↑, Treatment with Chaetocin resulted in ∼3–5-fold increase in caspase-3 activity
Trx1↓, Chaetocin decreases the expression of TRX-1 in glioma cells
H3↓, Chaetocin-mediated inhibition of histone H3 methylation is ROS dependent
lactateProd↓, Chaetocin decreases lactate levels, ATP production and glucose uptake in a ROS- and JNK-dependent manner
ATP↓,
GlucoseCon↓,
TumCG↓, Chaetocin inhibits growth of tumor xenograft in nude mice
Dose↝, 10 animals each and were administered either with vehicle or Chaetocin (0.5 mg/kg body weight), intraperitoneally on alternate days for 25 days.

8028- IVM,    Ivermectin as an Alternative Anticancer Agent: A Review of Its Chemical Properties and Therapeutic Potential
- Review, Var, NA
*BioAv↝, IVM’s distinct physicochemical profile, including high lipophilicity, poor aqueous solubility, and moderate acid stability, which collectively affect its bioavailability and pharmacokinetic behavior.
Apoptosis↑, induction of apoptosis, inhibition of tumor cell proliferation, and modulation of the tumor microenvironment across a range of malignancies.
TumCP↓,
Wnt↓, IVM inhibits the Wnt/β-catenin signaling pathway in gastric cancer cells, leading to suppressed tumor growth and metastasis.
β-catenin/ZEB1↓,
TumCG↓,
TumMeta↓,
PI3K↓, IVM disrupts the PI3K/AKT/mTOR pathway in pancreatic cancer, resulting in increased apoptosis and reduced cell proliferation.
Akt↓,
mTOR↓,
TumPF↓,
CSCs↓, IVM selectively suppresses CSCs in breast cancer models and downregulates genes associated with cellular stemness,
eff↑, combining IVM with immune checkpoint inhibitors, such as anti-PD1 antibodies, enhances antitumor immune responses and induces complete tumor regression in breast cancer models.
ChemoSen↑, Combination of Paclitaxel + Ivermectin or Paclitaxel + Pitavastatin produced maximum cytotoxicity and strong synergy in both chemoresistant lines, surpassing the effect of each drug alone
mtDam↑, IVM induces mitochondrial dysfunction (↓ψm, ↓ATP) with ↑ROS, inhibits NF-κB (↓p-p65), increases Bax/Bcl-2 and activates caspases 9/3
MMP↓,
ATP↓,
ROS↑,
NF-kB↓,
BAX↑,
Casp3↑,
Casp9↑,
ICD↑, induces immunogenic cell death
Ki-67↓, ↓Ki67, PSA
PSA↓,
YAP/TEAD↓, interferes with multiple oncogenic pathways, including WNT/TGF-β, PAK1/STAT3, YAP1, Akt/mTOR, and Wnt/β-catenin.

5099- JG,    Juglone induces ferroptosis in glioblastoma cells by inhibiting the Nrf2-GPX4 axis through the phosphorylation of p38MAPK
- vitro+vivo, GBM, LN229 - vitro+vivo, GBM, T98G
Ferroptosis↑, Juglone mainly causes cell death by inducing ferroptosis
p‑MAPK↑, juglone can significantly activate the phosphorylation of p38MAPK
NRF2↓, juglone induces the ferroptosis of GBM by activating the phosphorylation of p38MAPK and negatively regulating the Nrf2-GPX4 signaling pathway.
GPx4↓,
TumPF↓, Juglone significantly inhibits the proliferation of GBM cells and induces cell apoptosis
Apoptosis↑,
ROS↑, Juglone can dose-dependently enhance the accumulation of ROS in GBM cells
GSH↓, juglone can reduce the content of GSH
lipid-P↑, lipid peroxidation
Ki-67↓, The results show that juglone significantly inhibits the expression of Ki67, GPX4, and Nrf2
TumCG↓, juglone inhibits tumor growth in vivo by inducing ferroptosis.

8113- LA,    Analyzing of colorectal cancer related genes and microRNAs expression profiles in response to probiotics Lactobacillus acidophilus and Saccharomyces cerevisiae in colon cancer cell lines
- in-vitro, CRC, HT-29 - in-vitro, CRC, SW480
BAX↑, upregulation in the BAX, CASP3, and CASP9 and down regulation BCl-2, MMP2, and MMP9 genes
Casp3↑,
Casp9↑,
Bcl-2↓,
MMP2↓,
MMP9↓,
miR-34a↑, Also, a comparison of microRNA expression profiles indicated an increase of miR 34, 135, 25, 16, 195, 27, 98, let7 and a decrease of miR 9, 106b, 17, 21, 155, 221.
miR-25-5p↑,
miR-195↑,
miR-27a-3p↑,
Let-7↑,
miR-106b↓,
miR-17↓,
miR-21↓,
miR-155↓,
miR-221↓,
TumPF↓, The findings of this study indicate that probiotics can effectively suppress the proliferation of colorectal cancer cells and even reverse their development.


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

miR-106b↓, 1,   miR-195↑, 1,   SUV39H↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   ICD↑, 1,   lipid-P↑, 1,   NRF2↓, 1,   ROS↑, 3,   Trx1↓, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 2,   MMP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

GlucoseCon↓, 1,   lactateProd↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 2,   Bcl-2↓, 1,   Casp3↑, 3,   Casp9↑, 2,   Ferroptosis↑, 1,   p‑JNK↑, 1,   p‑MAPK↑, 1,   YAP/TEAD↓, 1,   YAP/TEAD↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

miR-25-5p↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

H3↓, 1,   miR-21↓, 1,   miR-27a-3p↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

p‑ATM↑, 1,  

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

CSCs↓, 1,   HMTs↓, 1,   Let-7↑, 1,   miR-34a↑, 1,   mTOR↓, 1,   PI3K↓, 1,   TumCG↓, 3,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

Ki-67↓, 2,   miR-155↓, 1,   miR-221↓, 1,   MMP2↓, 1,   MMP9↓, 1,   TumCP↓, 1,   TumMeta↓, 1,   TumPF↓, 4,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

miR-17↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NF-kB↓, 1,   PSA↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose↝, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Ki-67↓, 2,   PSA↓, 1,  
Total Targets: 58

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,  
Total Targets: 1

Scientific Paper Hit Count for: TumPF, Tumor-promoting fibroblasts
1 chaetocin
1 Ivermectin
1 Juglone
1 Lactobacillus
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#:329  State#:%  Dir#:1
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