Diff Cancer Research Results

Diff, differentiation: Click to Expand ⟱
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Differentiation refers to the process by which cells become specialized in structure and function.
-In healthy tissues, cells undergo differentiation to become specialized types (e.g., muscle cells, neurons, blood cells) that perform specific functions. This process is tightly regulated by genetic and epigenetic factors.
-In some cases, cells can lose their specialized characteristics, a process known as dedifferentiation. This is often seen in cancer, where tumor cells revert to a more primitive, less differentiated state.
Scientific Papers found: Click to Expand⟱
2686- BBR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Nor, NA
Inflam↓, BBR has documented to have anti-diabetic, anti-inflammatory and anti-microbial (both anti-bacterial and anti-fungal) properties.
IL6↓, BBRs can inhibit IL-6, TNF-alpha, monocyte chemo-attractant protein 1 (MCP1) and COX-2 production and expression.
MCP1↓,
COX2↓,
PGE2↓, BBRs can also effect prostaglandin E2 (PGE2)
MMP2↓, and decrease the expression of key genes involved in metastasis including: MMP2 and MMP9.
MMP9↓,
DNAdam↑, BBR induces double strand DNA breaks and has similar effects as ionizing radiation
eff↝, In some cell types, this response has been reported to be TP53-dependent
Telomerase↓, This positively-charged nitrogen may result in the strong complex formations between BBR and nucleic acids and induce telomerase inhibition and topoisomerase poisoning
Bcl-2↓, BBR have been shown to suppress BCL-2 and expression of other genes by interacting with the TATA-binding protein and the TATA-box in certain gene promoter regions
AMPK↑, BBR has been shown in some studies to localize to the mitochondria and inhibit the electron transport chain and activate AMPK.
ROS↑, targeting the activity of mTOR/S6 and the generation of ROS
MMP↓, BBR has been shown to decrease mitochondrial membrane potential and intracellular ATP levels.
ATP↓,
p‑mTORC1↓, BBR induces AMPK activation and inhibits mTORC1 phosphorylation by suppressing phosphorylation of S6K at Thr 389 and S6 at Ser 240/244
p‑S6K↓,
ERK↓, BBR also suppresses ERK activation in MIA-PaCa-2 cells in response to fetal bovine serum, insulin or neurotensin stimulation
PI3K↓, Activation of AMPK is associated with inhibition of the PI3K/PTEN/Akt/mTORC1 and Raf/MEK/ERK pathways which are associated with cellular proliferation.
PTEN↑, RES was determined to upregulate phosphatase and tensin homolog (PTEN) expression and decrease the expression of activated Akt. In HCT116 cells, PTEN inhibits Akt signaling and proliferation.
Akt↓,
Raf↓,
MEK↓,
Dose↓, The effects of low doses of BBR (300 nM) on MIA-PaCa-2 cells were determined to be dependent on AMPK as knockdown of the alpha1 and alpha2 catalytic subunits of AMPK prevented the inhibitory effects of BBR on mTORC1 and ERK activities and DNA synthes
Dose↑, In contrast, higher doses of BBR inhibited mTORC1 and ERK activities and DNA synthesis by AMPK-independent mechanisms [223,224].
selectivity↑, BBR has been shown to have minimal effects on “normal cells” but has anti-proliferative effects on cancer cells (e.g., breast, liver, CRC cells) [225–227].
TumCCA↑, BBR induces G1 phase arrest in pancreatic cancer cells, while other drugs such as gemcitabine induce S-phase arrest
eff↑, BBR was determined to enhance the effects of epirubicin (EPI) on T24 bladder cancer cells
EGFR↓, In some glioblastoma cells, BBR has been shown to inhibit EGFR signaling by suppression of the Raf/MEK/ERK pathway but not AKT signaling
Glycolysis↓, accompanied by impaired glycolytic capacity.
Dose?, The IC50 for BBR was determined to be 134 micrograms/ml.
p27↑, Increased p27Kip1 and decreased CDK2, CDK4, Cyclin D and Cyclin E were observed.
CDK2↓,
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↓,
Bax:Bcl2↑, Increased BAX/BCL2 ratio was observed.
Casp3↑, The mitochondrial membrane potential was disrupted and activated caspase 3 and caspases 9 were observed
Casp9↑,
VEGFR2↓, BBR treatment decreased VEGFR, Akt and ERK1,2 activation and the expression of MMP2 and MMP9 [235].
ChemoSen↑, BBR has been shown to increase the anti-tumor effects of tamoxifen (TAM) in both drug-sensitive MCF-7 and drug-resistant MCF-7/TAM cells.
eff↑, The combination of BBR and CUR has been shown to be effective in suppressing the growth of certain breast cancer cell lines.
eff↑, BBR has been shown to synergize with the HSP-90 inhibitor NVP-AUY922 in inducing death of human CRC.
PGE2↓, BBR inhibits COX2 and PEG2 in CRC.
JAK2↓, BBR prevented the invasion and metastasis of CRC cells via inhibiting the COX2/PGE2 and JAK2/STAT3 signaling pathways.
STAT3↓,
CXCR4↓, BBR has been observed to inhibit the expression of the chemokine receptors (CXCR4 and CCR7) at the mRNA level in esophageal cancer cells.
CCR7↓,
uPA↓, BBR has also been shown to induce plasminogen activator inhibitor-1 (PAI-1) and suppress uPA in HCC cells which suppressed their invasiveness and motility.
CSCs↓, BBR has been shown to inhibit stemness, EMT and induce neuronal differentiation in neuroblastoma cells. BBR inhibited the expression of many genes associated with neuronal differentiation
EMT↓,
Diff↓,
CD133↓, BBR also suppressed the expression of many genes associated with cancer stemness such as beta-catenin, CD133, NESTIN, N-MYC, NOTCH and SOX2
Nestin↓,
n-MYC↓,
NOTCH↓,
SOX2↓,
Hif1a↓, BBR inhibited HIF-1alpha and VEGF expression in prostate cancer cells and increased their radio-sensitivity in in vitro as well as in animal studies [290].
VEGF↓,
RadioS↑,

5223- EMD,    Emodin inhibits colon cancer by altering BCL-2 family proteins and cell survival pathways
- in-vitro, CRC, DLD1 - in-vitro, Nor, CCD841
tumCV↓, Emodin decreased viability of CoCa cells and induced apoptosis in a time and dose-dependent manner compared to vehicle-treated control without significantly impacting normal colon epithelial cells.
Apoptosis↑,
selectivity↑,
Casp↑, Emodin activated caspases, modulated Bcl-2 family of proteins and reduced mitochondrial membrane potential to induce CoCa cell death
Bcl-2↓,
MMP↓,
TumCD↑,
MAPK↓, Signaling (MAPK/JNK, PI3K/AKT, NF-κβ and STAT) pathways associated with cell growth, differentiation, and Bcl-2 family expression or function were negatively regulated by Emodin.
JNK↓,
PI3K↓,
Akt↓,
NF-kB↓,
STAT↓,
Diff↓,
P53↑, significant increase in p53 and decrease in PARP protein levels in response to Emodin treatment.
PARP↓,

218- MFrot,  MF,    Extremely low frequency magnetic fields inhibit adipogenesis of human mesenchymal stem cells
- in-vitro, Nor, NA
*PPARγ↓, PPARg2
*p‑JNK↑, p-JNK
*Wnt↑,
*ALP∅, ELF-MF had no effects on the expression of ALP, COL1a1, Runx2, and OCN
*COL1∅,
*RUNX2∅,
*OCN∅,
*FABP4↓, ELF-MF exposure for 15 days resulted in a decrease in PPARg2 and FABP4
*p‑JNK↑, p-JNK was increased after ELF-MF exposure
*Diff↓, adipogenic differentiation of MSCs could be inhibited by ELF-MF of 7.5 Hz, 0.4 T, suggesting the inhibitory effect of ELF-MF on obesity may be attributed to the inhibition of differentiation of MSCs into adipocytes.

5016- PEITC,    Phenethyl Isothiocyanate (PEITC) interaction with Keap1 activates the Nrf2 pathway and inhibits lipid accumulation in adipocytes
- in-vitro, Nor, NA
*NRF2↑, Phenethyl Isothiocyanate (PEITC) interaction with Keap1 activates the Nrf2 pathway and inhibits lipid accumulation in adipocytes
*Diff↓, PEITC was found to activate Nrf2-mediated gene expression and inhibit adipocyte differentiation, at least partially, through Nrf2-dependent mechanisms.
*Weight↓, Administration of PEITC in high-calorie diet-fed mice reduced body weight, epididymal fat weight, and hepatic lipid contents
*lipid-P↓,

3380- QC,    Quercetin as a JAK–STAT inhibitor: a potential role in solid tumors and neurodegenerative diseases
- Review, Var, NA - Review, Park, NA - Review, AD, NA
JAK↓, plant polyphenols, especially quercetin, exert their inhibitory effects on the JAK–STAT pathway through known and unknown mechanisms.
STAT↓,
Inflam↓, quercetin significantly reduced levels of inflammation moderators, including NO synthase, COX-2, and CRP, in a human hepatocyte-derived cell line
NO↓,
COX2↓,
CRP↓,
selectivity↑, , quercetin is not harmful to healthy cells, while it can impose cytotoxic effects on cancer cells through a variety of mechanisms,
*neuroP↑, Alzheimer’s disease because of its antioxidant and anti-inflammatory activity.
STAT3↓, demonstrated as a suppressor of the STAT3 activation signaling pathway
cycD1/CCND1↓, Rb phosphorylation, cyclin D1 expression, and MMP-2 secretion are inhibited by 48 h treatment with 25 µM quercetin in T98G and U87 GBM cell lines
MMP2↓,
STAT4↓, by inhibiting IL-12-induced tyrosine phosphorylation of STAT3, STAT4, JAK2, and TYK2, quercetin inhibits the proliferation of T cells and differentiation of Th1
JAK2↓,
TumCP↓,
Diff↓,
*eff↑, administration of quercetin with piperine alone and in combination significantly prevented neuroinflammation via reducing the levels of IL-6, TNF-α (two potent activators of the JAK–STAT pathway), and IL-1β in PD in experimental rats
*IL6↓,
*TNF-α↓,
*IL1β↓,
*Aβ↓, quercetin suppressing β-secretase (an enzyme engaged in Aβ formation) and aggregation of Aβ

3198- SFN,    Sulforaphane and TRAIL induce a synergistic elimination of advanced prostate cancer stem-like cells
- in-vitro, Pca, NA
Nanog↓, sulforaphane reduced the amount of Nanog, Sox2, E-cadherin, GATA-4, HNF-3β, SOX17, Otx2, TP63, Snail, VEGF R2 and HCG.
SOX2↓,
E-cadherin↓,
Snail↓,
VEGFR2↓,
Diff↓, sulforaphane, particularly in combination with TRAIL, reduces the levels of proteins required for self-renewal, differentiation, cell migration, the epithelialmesenchymal transition (EMT) and tumorigenesis (
TumCMig↓,
EMT↓,
CXCR4↓, CXCR4 receptor, which is involved in migration and metastasis (42), was inhibited following the sulforaphane-only treatment
NOTCH1↓, Similar results were found for the Notch 1 receptor
ALDH1A1↓, Sulforaphane significantly reduced the ALDH1 activity from ∼30 to 12%; conversely
CSCs↓, data suggest that sulforaphane strongly inhibits stem cell signaling
eff↑, demonstrated that sulforaphane and TRAIL reduced the expression of the CSC markers CD133, CXCR4, Nanog, c-Met, EpCAM, CD44, and ALDH1 and the proliferation marker Ki67;


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 ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MEK↓, 1,   MMP↓, 2,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   Glycolysis↓, 1,   p‑S6K↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Casp↑, 1,   Casp3↑, 1,   Casp9↑, 1,   JNK↓, 1,   MAPK↓, 1,   p27↑, 1,   Telomerase↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   PARP↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH1A1↓, 1,   CD133↓, 1,   CSCs↓, 2,   Diff↓, 4,   EMT↓, 2,   ERK↓, 1,   p‑mTORC1↓, 1,   n-MYC↓, 1,   Nanog↓, 1,   Nestin↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   PI3K↓, 2,   PTEN↑, 1,   SOX2↓, 2,   STAT↓, 2,   STAT3↓, 2,   STAT4↓, 1,  

Migration ⓘ

E-cadherin↓, 1,   MMP2↓, 2,   MMP9↓, 1,   Snail↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   uPA↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   Hif1a↓, 1,   NO↓, 1,   VEGF↓, 1,   VEGFR2↓, 2,  

Immune & Inflammatory Signaling ⓘ

CCR7↓, 1,   COX2↓, 2,   CRP↓, 1,   CXCR4↓, 2,   IL6↓, 1,   Inflam↓, 2,   JAK↓, 1,   JAK2↓, 2,   MCP1↓, 1,   NF-kB↓, 1,   PGE2↓, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose?, 1,   Dose↓, 1,   Dose↑, 1,   eff↑, 4,   eff↝, 1,   RadioS↑, 1,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

CRP↓, 1,   EGFR↓, 1,   IL6↓, 1,  
Total Targets: 81

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

lipid-P↓, 1,   NRF2↑, 1,  

Core Metabolism/Glycolysis ⓘ

FABP4↓, 1,   PPARγ↓, 1,  

Cell Death ⓘ

p‑JNK↑, 2,  

Kinase & Signal Transduction ⓘ

OCN∅, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↓, 2,   RUNX2∅, 1,   Wnt↑, 1,  

Migration ⓘ

COL1∅, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   IL6↓, 1,   TNF-α↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

ALP∅, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

neuroP↑, 1,   Weight↓, 1,  
Total Targets: 19

Scientific Paper Hit Count for: Diff, differentiation
1 Berberine
1 Emodin
1 Magnetic Field Rotating
1 Magnetic Fields
1 Phenethyl isothiocyanate
1 Quercetin
1 Sulforaphane (mainly Broccoli)
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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