CSCs Cancer Research Results

CSCs, Cancer Stem Cells: Click to Expand ⟱
Source:
Type:
Cancer Stem Cells

Phytochemicals (natural plant-derived compounds) that may affect CSCs:
Curcumin
— suppresses self-renewal and pathways (Wnt/Notch/Hedgehog).
Resveratrol
— shown to reduce CSC populations and sphere formation in multiple models.
Sulforaphane (from broccoli sprouts)
— reported to inhibit CSC properties and pathways; active in vitro and in vivo.
EGCG (epigallocatechin-3-gallate, green tea)
— reduces CSC markers and sphere formation in several cancer types.
Quercetin
— reported to inhibit CSC proliferation, self-renewal and invasiveness (breast, endometrial, others).
Berberine
— shown to suppress CSC “stemness” and reduce tumorigenic properties in multiple models.
Genistein (soy isoflavone)
— decreases CSC markers, sphere formation and stemness signaling in prostate/breast/other models.
Honokiol (Magnolia bark)
— shown to eliminate or suppress CSC-like populations in oral, colon, glioma models.
Luteolin
— inhibits stemness/EMT and reduces CSC markers and self-renewal in breast, prostate and other models.
Withaferin A (from Withania somnifera / ashwagandha)
— multiple preclinical reports show WA targets CSCs and reduces tumor growth/metastasis in models.

Circadian disruption in cancer and regulation of cancer stem cells by circadian clock genes: An updated review
Potential Role of the Circadian Clock in the Regulation of Cancer Stem Cells and Cancer Therapy
Can we utilise the circadian clock to target cancer stem cells?
Scientific Papers found: Click to Expand⟱
7887- VT,  IVT,    Dietary Flavonoids Vitexin and Isovitexin: New Insights into Their Functional Roles in Human Health and Disease Prevention
- Review, AD, NA - Review, Var, NA
*antiOx↑, antioxidant, anti-inflammatory, anticancer, antibacterial, and neuroprotective mechanisms.
*Inflam↓,
*AntiCan↑,
*Bacteria↓,
*neuroP↑, cardiovascular protection, blood sugar regulation, anti-obesity, anticancer, antioxidant, anti-inflammatory, and neuroprotective properties.
*Obesity↓,
*cardioP↑, Vitexin exerts a cardioprotective effect against DOX-induced cardiac toxicity by reducing oxidative stress, lowering cardiac inflammatory cytokines, increasing FOXO3a, and inhibiting caspase-3 activation.
*ROS↓, Sprague-Dawley rat hearts, H9c2 cells 10 μM Reducing ROS levels; improving mitochondrial activity, mitochondrial membrane potential, and ATP content; markedly increasing MFN2 expression and reducing the recruitment of Drp1 in mitochondria.
*MMP↑,
*ATP↑,
*MFN2↑,
*DRP1/DNM1L↓,
*FOXO3↑, Protect against DOX-induced acute cardiotoxicity Rats 30 mg/kg Vitexin induced elevated FOXO3a protein expression levels, by suppressing oxidative stress
*NRF2↑, vitexin activated nuclear factor-erythroid 2-related factor 2 (Nrf2) in HUVEC under high glucose.
*Ferroptosis↓, Diabetic nephropathy HK-2 cells/DN rat 0–40 μM Vitexin could alleviate diabetic nephropathy by attenuated ferroptosis via activating GPX4
*GPx4↑,
TumCP↓, Gastric cancer Nude mice/GC cells 2 mg/kg 10–160 μM Vitexin inhibited the malignant progression of GC in vitro and in vivo by suppressing HMGB1-mediated activation of PI3K/Akt/HIF-1α signaling pathway.
HMGB1↓,
PI3K↓,
Akt↓,
Hif1a↓,
CDK1↓, Colon cancer HCT-116 cells 1–300 μM Inhibit colon cancer HCT-116 cell proliferation by suppressing CDK1/cyclin B expression, leading to cell cycle arrest in the G2/M phase.
CycB/CCNB1↓,
TumCCA↑,
Apoptosis↑, Isovitexin Colon cancer Promoted apoptosis and suppressed cell proliferation by activating the p53 signaling pathway.
P53↑,
NF-kB↓, Non-small cell lung cancer cells A549/ H1299 cells, nude mice 1–120 μM Suppressed NF-κB, AKT and ERK activation. [24] Vitexin A549 cells, nude mice 0–40 μM Reduced the levels of p-PI3K, p-Akt, and p-mTOR.
ERK↓,
p‑PI3K↓,
miR-34a↑, Isovitexin Hepatocarcinoma SK-Hep-1 cells Mediated miR-34a upregulation induces apoptosis and suppresses the stemness of SK-SC.
Apoptosis↑,
CSCs?,
*MAPK↓, Isovitexin Acute lung injury RAW 264.7 cells 0–50 μM Inhibiting MAPK and NF-κB and activating HO-1/Nrf2 pathways.
*HO-1↑,
*hepatoP↑, EAH mice 5 mg/kg Vitexin ameliorated hepatic injury in EAH mice through activation of the AMPK/AKT/GSK-3β pathway and upregulation of the Nrf2 gene.
*AMPK↑,
*Akt↑,
*GSK‐3β↑,
*chemoP↑, Vitexin exerts a cardioprotective effect against DOX-induced cardiac toxicity by reducing oxidative stress, lowering cardiac inflammatory cytokines, increasing FOXO3a, and inhibiting caspase-3 activation.
*Casp3↓,
*IRes↝, Vitexin and isovitexin flavonoids not only affected the absorption of peripheral glucose in insulin and non-insulin sensitive tissues but also showed the potential to restore insulin resistance in HepG2 cells by enhancing cellular uptake of glucose.
*GlucoseCon↑,
ChemoSen↑, When combined with doxorubicin (Dox), vitexin can reduce tumor growth and show synergistic effects in in vivo tests, increasing antitumor efficacy.
*GSH↑, Vitexin also increased Nrf2 expression and boosted GSH and antioxidant enzymes such as SOD, CAT, GPx, and GST.
*SOD↑,
*ATF2↑,
*GPx↑,
*GSTs↑,
*AntiAge↑, In Caenorhabditis elegans, studies have shown that vitexin and isovitexin, as putative SKN-1/Nrf2 activators, increase lifespan and support a healthy lifespan.
*Stroke↓, It has been demonstrated that vitexin protects against a cerebral ischemia/reperfusion (I/R)-induced increase in the permeability of brain endothelial cells
*AChE↓, vitexin treatment significantly inhibited acetylcholinesterase activity and markedly downregulated the expression of ace-1 and ace-2.
*ACE/ACE1↓,
*ACE2↓,
*GutMicro↑, Vitexin and isovitexin have also shown promising potential in modulating intestinal microbiota and in turn play a significant role in regulating various diseases such as overweight
*MPO↓, Vitexin can also resist Helicobacter pylori infection, which may be related to its anti-myeloperoxidase (MPO) enzyme activity and inhibition of H- and K-ATPase activity
*H+/K+-ATPase↓,
*AntiDiabetic↑, Antidiabetic Vitexin and Isovitexin Inhibits α-glucosidase/α-amylase, promotes GLUT4, modulates gut microbiota
*GLUT4↑,
*Obesity↓, Anti-obesity Vitexin Activates AMPKα, inhibits C/EBPα, FAS, activates Hedgehog signaling
*HH↓,
*RenoP↑, vitexin protects the kidneys and prevents the formation of kidney stones by inhibiting pyroptosis, apoptosis, epithelial–mesenchymal transition (EMT), and macrophage activation.
*BioAv↓, Vitexin and isovitexin have poor absorption in the gastrointestinal tract, with significant first-pass effects in the intestine (approximately 94%), stomach (30%), and liver (50%), resulting in a lower bioavailability (F) (approximately 5%).
*BioAv↝, The absorption and metabolism processes of vitexin and isovitexin in the human body are complex, and their bioavailability is influenced by multiple factors, including the action of the gut microbiota, interactions with dietary components, first-pass
*BioAv↑, The vitexin-loaded bilayer nanoparticles are designed by assembling soybean peptides and coating them with a goblet cell-targeting peptide. They significantly increase the bioaccessibility and bioavailability of vitexin


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 2,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CycB/CCNB1↓, 1,   TumCCA↑, 1,  

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

CSCs?, 1,   ERK↓, 1,   miR-34a↑, 1,   PI3K↓, 1,   p‑PI3K↓, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

HMGB1↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,  
Total Targets: 16

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

ACE/ACE1↓, 1,   ACE2↓, 1,   H+/K+-ATPase↓, 1,   IRes↝, 1,   Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Ferroptosis↓, 1,   GPx↑, 1,   GPx4↑, 1,   GSH↑, 1,   GSTs↑, 1,   HO-1↑, 1,   MFN2↑, 1,   MPO↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   DRP1/DNM1L↓, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   GlucoseCon↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   ATF2↑, 1,   Casp3↓, 1,   Ferroptosis↓, 1,   MAPK↓, 1,  

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

FOXO3↑, 1,   GSK‐3β↑, 1,   HH↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT4↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioAv↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   Obesity↓, 2,   RenoP↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 47

Scientific Paper Hit Count for: CSCs, Cancer Stem Cells
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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