selectivity Cancer Research Results

selectivity, selectivity: Click to Expand ⟱
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The selectivity of cancer products (such as chemotherapeutic agents, targeted therapies, immunotherapies, and novel cancer drugs) refers to their ability to affect cancer cells preferentially over normal, healthy cells. High selectivity is important because it can lead to better patient outcomes by reducing side effects and minimizing damage to normal tissues.

Achieving high selectivity in cancer treatment is crucial for improving patient outcomes. It relies on pinpointing molecular differences between cancerous and normal cells, designing drugs or delivery systems that exploit these differences, and overcoming intrinsic challenges like tumor heterogeneity and resistance

Factors that affect selectivity:
1. Ability of Cancer cells to preferentially absorb a product/drug
-EPR-enhanced permeability and retention of cancer cells
-nanoparticle formations/carriers may target cancer cells over normal cells
-Liposomal formations. Also negatively/positively charged affects absorbtion

2. Product/drug effect may be different for normal vs cancer cells
- hypoxia
- transition metal content levels (iron/copper) change probability of fenton reaction.
- pH levels
- antiOxidant levels and defense levels

3. Bio-availability
Scientific Papers found: Click to Expand⟱
6352- DRE,    Investigation of the Anti-Lung Cancer Mechanisms of Taraxacum officinale Based on Network Pharmacology and Multidimensional Experimental Validation
- in-vitro, Lung, A549 - in-vitro, Nor, L929
other↝, Our analyses identified 58 active compounds in dandelion linked to 614 potential targets, of which 228 targets were associated with LC.
other↝, six key targets—TP53, CASP3, EGFR, AKT1, ESR1, and NQO1—were selected for molecular docking with four major active compounds: quercetin, apigenin, kaempferol, and luteolin.
tumCV↑, viability of A549 cells progressively decreased with increasing taraxasterol concentration and treatment duration, with the most significant inhibitory effect observed at 25 μmol/L
selectivity?, At the same concentration, taraxasterol did not exhibit significant cytotoxicity toward normal L929 cells, with cell viability remaining at or above 80%
EGFR↓, six hub genes—TP53, CASP3, EGFR, AKT1, ESR1, and NQO1—were identified as potential key targets underlying the anti-lung cancer effects of dandelion.
AKT1↓,
NQO1↓,

8090- KAE,    A systematic review of anti-cancer roles and mechanisms of kaempferol as a natural compound
- Review, Nor, NA
*cardioP↑, kaempferol has been linked to various cardiovascular, cancer, inflammatory, neurodegenerative, and obese diseases
*AntiCan↑,
*Inflam↓,
*neuroP↑,
*BioAv↓, in a 2002 study by Radtke, the plasma concentration of kaempferol was reported to be 10.7 nM, while the intake amount was 4.7 mg/day
selectivity?, Their study showed that kaempferol was a potent inhibitor in bladder cancer with high safety on normal cells.
p‑Akt↓, it suppressed the phosphorylation of AKT, CyclinD1, CDK4, Bid, Mcl-1, and Bcl-xL, while boosting the expression of p-BRCA1, ATM, p53, p21, and p38, as well as Bax and Bid.
p‑cycD1/CCND1↓,
p‑CDK4↓,
p‑BID↓,
p‑Mcl-1↓,
p‑BRCA1↑,
ATM↑,
P53↑,
P21↑,
p38↑,
BAX↑,
BID↑,
MMP↓, decrease mitochondrial membrane potential and increase caspase-3, -7, and -9 activities in the U-2 OS cell line.
Casp3↑,
Casp7↑,
Casp9↑,
AIF↑, A rise in AIF protein levels was also observed, indicating that apoptosis was induced through a caspase-independent mitochondrial mechanism.
ER Stress↑, The endoplasmic reticulum stress pathways are the other mechanism induced by kaempferol in the human osteosarcoma cell line.
TumMeta↓, kaempferol inhibited cell metastasis in U-2 OS cells by inhibiting various signaling pathways (e.g., ERK, AP-1, JNK, and p38)
ERK↓,
AP-1↓,
JNK↓,
p38↓,
GLUT1↓, suggested chemoprotective mechanism of kaempferol can result in toxicity and proliferation arrest due to the downregulation of glucose transporter 1 (GLUT1) gene expression and inhibition of cellular glucose uptake in cancer cell lines.
GlucoseCon↓,
MMP9↓, Downregulation of the matrix metalloproteinase-9 (MMP) expression and activity was the other process in breast cancer invasion treated with kaempferol using the MDA-MB-231 cell line
CYP1A1↓, kaempferol influenced the aryl hydrocarbon receptor in inhibiting CYP1A1 transcription
ChemoSen↑, Cancer stem cell markers, such as Oct-4, Nanog, ABCB1, and ALDH1A1, were significantly reduced in MCF-7 cells treated with kaempferol and docetaxel.
OCT4↓,
Nanog↓,
P-gp/ABCB1↓,
ALDH1A1↓,
TumCCA↑, Kaempferol could also suppress the proliferation of triple-negative breast cancer, contribute to the G2/M arrest induction, induce apoptosis and DNA damage, increase the expression of γ-H2AX and cleave the caspase-9, caspase-3, and p-ATM
DNAdam↑,
γH2AX↑,
COX2/PTGS2↓, The new derivative showed downregulation of the expression of COX-2, inhibited migration, decreased intracellular ROS and calcium cation levels, decreased Bcl-2 expression, and increased Bax expression in MCF-7 cells
i-ROS↓,
Ca+2↓,
eff↑, The activation of death receptor 5 (DR5) by kaempferol increased the sensitivity of colon cancer cells to TRAIL-induced apoptosis
DR5↑,
ChemoSen↑, combination of doxorubicin (DOX) and kaempferol was more efficient in induction of apoptosis and cytotoxic effect against HT-29 colon cancer cell line in comparison with each drug alone
Akt↓, kaempferol inhibits PI3K/Akt signaling pathways
PI3K↓,
ROS↑, rat model of hepatocellular carcinoma through the mitochondrial-dependent pathway by targeting upstream activities such as the enhancement of ROS formation, MMP downregulation, and the increasing of the caspase-3 activity in the cytosol
EMT↓, kaempferol inhibits the EMT, migration, and MMP-2 activation induced by TGF-1 in these cancer cells
survivin↓, Kaempferol was also responsible for downregulating phosphorylated Akt and reducing the quantity of survivin protein to stop survivin

8238- LCA,    Licochalcone A is a Natural Selective Inhibitor of Arginine Methyltransferase 6
- in-vitro, BC, MCF7 - in-vivo, NA, MCF10
PRMT6↓, Here, we describe the identification of a natural compound, licochalcone A, as a novel, reversible and selective inhibitor of PRMT6.
EstroRS/ERS↓, In MCF-7 cells, it inhibited PRMT6-dependent methylation of histone H3 at arginine 2 (H3R2), which resulted in a significant repression of estrogen receptor activity.
selectivity?, Licochalcone A exhibited cytotoxicity towards human MCF-7 breast cancer cells, but not MCF-10A human breast epithelial cells, by up-regulating p53 expression and blocking cell cycle progression at G2/M, followed by apoptosis.
P53↑,
TumCCA↑,
Apoptosis↑,

1994- PTL,    Parthenolide Inhibits Tumor Cell Growth and Metastasis in Melanoma A2058 Cells
- in-vitro, Melanoma, A2058 - in-vitro, Nor, L929
tumCV↓, PAR significantly reduced the viability of A2058 cancer cells
selectivity?, demonstrating greater potency against cancer cells compared to normal L929 cells (IC50: 20 μM vs. 27 μM after 24h
ROS?, PAR increased ROS production
BAX↑, elevated mRNA expression of pro-apoptotic Bax and NME1 genes
TumCCA?, PAR induced apoptosis and cell cycle arrest in A2058 cells, as evidenced by the increased proportion of cells in the late apoptotic phase and sub-G1 cell cycle arrest
MMP2↓, MMP-2 and MMP-9 mRNA and protein expressions, gelatinase activity, and the migration of A2058 cells were also decreased by PAR
MMP9↓,
TumCMig↓,
eff↑, These results, along with the synergic effect with dacarbazine, indicated that PAR may have the potential to be a therapeutic drug for melanoma by triggering apoptosis and suppressing invasion and migration.

1494- SFN,  doxoR,    Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model
- in-vivo, BC, NA - in-vitro, BC, MCF7 - in-vitro, Nor, MCF10
CardioT↓, SFN (4 mg/kg, 5 days/week) protected against mortality and cardiac dysfunction induced by DOX
*GSH↑, Rats Hearts: SFN and DOX co-treatment reduced MDA and 4-HNE adduct formation and also prevented DOX-induced depletion of GSH levels
*ROS↓, SFN reduces DOX-induced oxidative stress in the heart of non-tumor bearing rats.
*NRF2↑, activates Nrf2 in rat hearts during DOX treatment
NRF2∅, SFN does not interfere with DOX toxicity or Nrf2 activity in breast cancer cell lines
HDAC↓, SFN acts synergistically with DOX to inhibit HDAC and DNMT activity, decrease ERα detection and increase caspase-3 activity
DNMTs↓,
Casp3↑,
ER-α36↓, ERα levels in MCF-7, MDA-MB-231
Remission↑, SFN+DOX treatment (with a total DOX dose of 20 mg/kg) was able to eradicate the tumors in all rats by day 35 after tumor implantation
eff↑, SFN (4 mg/kg oral; 5 days/week for 5 weeks) with DOX (total of 10 or 20 mg/kg i.p. administered over 4 weeks) and showed that in combination with SFN, the dosage of DOX could be < by 50% while still eliciting the same anti-cancer effects as DOX alone
ROS↑, Increased generation of reactive oxygen species (ROS), an altered redox status, and aerobic glycolysis for energy production distinguish highly proliferative cancer cells from normal healthy cells
selectivity?, ROS production... distinguish highly proliferative cancer cells from normal healthy cells


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

PRMT6↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

CYP1A1↓, 1,   NQO1↓, 1,   NRF2∅, 1,   ROS?, 1,   ROS↑, 2,   i-ROS↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AKT1↓, 1,   GlucoseCon↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 2,   BID↑, 1,   p‑BID↓, 1,   Casp3↑, 2,   Casp7↑, 1,   Casp9↑, 1,   DR5↑, 1,   JNK↓, 1,   p‑Mcl-1↓, 1,   p38↓, 1,   p38↑, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 2,   tumCV↓, 1,   tumCV↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,   p‑BRCA1↑, 1,   DNAdam↑, 1,   DNMTs↓, 1,   P53↑, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

p‑CDK4↓, 1,   p‑cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA?, 1,   TumCCA↑, 2,  

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

ALDH1A1↓, 1,   EMT↓, 1,   ERK↓, 1,   HDAC↓, 1,   Nanog↓, 1,   OCT4↓, 1,   PI3K↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   Ca+2↓, 1,   ER-α36↓, 1,   MMP2↓, 1,   MMP9↓, 2,   TumCMig↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,   P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

EstroRS/ERS↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 2,   eff↑, 3,   selectivity?, 5,  

Clinical Biomarkers(tgid=22) ⓘ

p‑BRCA1↑, 1,   EGFR↓, 1,   EstroRS/ERS↓, 1,  

Functional Outcomes(tgid=23) ⓘ

CardioT↓, 1,   Remission↑, 1,  
Total Targets: 68

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

GSH↑, 1,   NRF2↑, 1,   ROS↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   cardioP↑, 1,   neuroP↑, 1,  
Total Targets: 8

Scientific Paper Hit Count for: selectivity, selectivity
1 Dandelion Root
1 Kaempferol
1 Licochalcone A
1 Parthenolide
1 Sulforaphane (mainly Broccoli)
1 doxorubicin
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#:1110  State#:%  Dir#:0
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