ABCG2 Cancer Research Results

ABCG2, BCRP/ATP-binding cassette sub-family G member 2: Click to Expand ⟱
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ATP-binding cassette sub-family G member 2 (ABCG2) is a protein that plays a crucial role in the transport of various substances across cell membranes, including drugs, lipids, and xenobiotics. ABCG2 is often high and associated with poor prognosis.

BCRP (ABCG2; breast cancer resistance protein) is an ATP-binding cassette efflux transporter that can export multiple anticancer drugs from cancer cells. In tumors, increased BCRP activity may lower intracellular drug accumulation and contribute to multidrug resistance, reduced chemotherapy response, and survival of resistant cancer stem-like or side-population cells. Therefore, for anti-cancer interpretation, BCRP/ABCG2 downregulation or inhibition is generally favorable when the therapeutic goal is to increase intracellular exposure to BCRP-substrate drugs. However, BCRP also protects normal tissues such as intestinal epithelium, liver, kidney, placenta, and blood-brain barrier, so systemic inhibition may alter drug distribution and toxicity.



Scientific Papers found: Click to Expand⟱
6137- CHr,    Effects of Chrysin and Its Major Conjugated Metabolites Chrysin-7-Sulfate and Chrysin-7-Glucuronide on Cytochrome P450 Enzymes and on OATP, P-gp, BCRP, and MRP2 Transporters
- in-vitro, NA, NA
CYP2C9↓, chrysin conjugates are strong inhibitors of certain biotransformation enzymes (e.g., CYP2C9) and transporters (e.g., OATP1B1, OATP1B3, OATP2B1, and BCRP) examined.
OATPs↓,
ABCG2↓,
BioEnh↝, simultaneous administration of chrysin-containing dietary supplements with medications needs to be carefully considered due to the possible development of pharmacokinetic interactions.

6703- DFC,    Molecular docking of anti-inflammatory drug diclofenac with metabolic targets: Potential applications in cancer therapeutics.
- Analysis, Var, NA
*Inflam?, NSAID diclofenac, 2-[2-(2,6-dichloroanilino)phenyl]acetic acid, which is conventionally used in clinical practice as a potent anti-inflammatory drug, owing to its proven safety records is also being tested for its antineoplastic potential
*COX1↓, anti-inflammatory action of diclofenac has been mainly attributed to its ability to inhibit prostaglandin-endoperoxide synthase-1 and 2 (PGES), commonly known as Cyclooxygenase-1 and 2
*COX2/PTGS2↓,
GLUT1↓, our results of docking analysis indicated optimum binding strength of diclofenac with targets in following order GLUT1, MCT4, LDH A, COX1, BCRP/ABCG2, HDM2/MDM2, COX2, MRP1, MnSOD/SOD2, Myc, β-Catenin, VEGF, IκB, c-Jun and E2F1.
MCT4↓,
LDHA↓,
ABCG2↓,
MDM2↓,
MRP1/ABCC1↓,
SOD2↓,
Myc↓,
β-catenin/ZEB1↓,
VEGF↓,
IKKα↓,
cJun↓,
E2Fs↓,

816- GAR,    Garcinol downregulates Notch1 signaling via modulating miR-200c and suppresses oncogenic properties of PANC-1 cancer stem-like cells
- in-vitro, PC, PANC1
Mcl-1↓,
EZH2↓,
ABCG2↓,
Gli1↓,
NOTCH1↓,
miR-200c↑, miR-200c increased by garcinol treatment was found to target and downregulate Notch1.

7787- ISL,    Dietary compound isoliquiritigenin targets GRP78 to chemosensitize breast cancer stem cells via β-catenin/ABCG2 signaling
- in-vitro, BC, NA
β-catenin/ZEB1↓, isoliquiritigenin (ISL) blocked β-catenin transcription activity with the highest inhibition ratio.
ChemoSen↑, ISL could have synergistic effects with chemotherapeutic drugs to inhibit breast cancer cell proliferation and colony formation.
CSCs↓, In addition, ISL could significantly limit the side population and CSC ratios in breast cancer cells, accompanied by inhibited self-renewal and multidifferentiation abilities
ABCG2↓, ISL could inhibit β-catenin/ABCG2 signaling by activating the proteasome degradation pathway
Proteasome↓,
GRP78/BiP↓, functional studies demonstrated that ISL could dock into the ATP domain of GRP78 and thereby inhibit its ATPase activity, resulting in its dissociation from β-catenin
selectivity↑, with little toxicity in normal tissues and mammary stem cells.

7894- IVT,    Isovitexin Inhibits Stemness and Induces Apoptosis in Hepatocellular Carcinoma SK-Hep-1 Spheroids by Upregulating miR-34a Expression
- in-vitro, HCC, SK-HEP-1
CD44↓, ISOV suppressed sphere and colony formation, and decreased CD44+ cell populations
CSCs↓,
ABCG2↓, ABCG2, ALDH1, and NANOG mRNA levels were decreased, while there was a concomitant increase in miR-34a levels
ALDH1A1↓,
Nanog↓,
miR-34a↑,
BAX↑, ISOV increased Bax protein levels, and reduced Bcl-2 and Mcl-1 protein levels in SK-SC
Bcl-2↓,
Mcl-1↓,
Apoptosis↑, We suggest that ISOV-mediated miR-34a upregulation induces apoptosis and suppresses the stemness of SK-SC.

61- QC,    Midkine downregulation increases the efficacy of quercetin on prostate cancer stem cell survival and migration through PI3K/AKT and MAPK/ERK pathway
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, ARPE-19
p‑PI3K↓, combined therapy inhibited the phosphorylation of PI3K, AKT and ERK1/2, and reduced the protein expression of p38, ABCG2 and NF-κB.
p‑Akt↓,
p‑ERK↓,
NF-kB↓,
p38↓,
ABCG2↓,
CD44↓, Quercetin alone exhibited significant cytotoxic effects on CD44+/CD133+
CD133↓,
CSCs↓,

5337- TFdiG,    Theaflavin 3,3'-digallate suppresses metastasis and reduces insulin-like growth factor-1-induced cancer stemness and invasiveness in human melanoma cells
- in-vitro, Melanoma, A375 - in-vitro, Melanoma, A2058
TumCMig↓, TF3 significantly inhibited cell migration, invasion, and matrix metalloproteinase (MMP) activity in A 375 and A2058 melanoma cells.
TumCI↓,
MMPs↓,
ALDH↓, It also suppressed sphere formation, self-renewal capacity, and aldehyde dehydrogenase 1 (ALDH1) activity.
CSCs↓, TF3 downregulated key cancer stemness and drug resistance markers, including ABCB1, ABCG2, CD44, and CXCR4.
ABCG2↓,
CD44↓,
CXCR4↓,
TumCG↓, In vivo, TF3 significantly inhibited tumor growth, reduced angiogenic marker expression, and suppressed lung metastasis.
angioG↓,
TumMeta↓,


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

SOD2↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

LDHA↓, 1,   MCT4↓, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Mcl-1↓, 2,   MDM2↓, 1,   Myc↓, 1,   p38↓, 1,   Proteasome↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↓, 1,   EZH2↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

GRP78/BiP↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

E2Fs↓, 1,  

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

ALDH↓, 1,   ALDH1A1↓, 1,   CD133↓, 1,   CD44↓, 3,   CSCs↓, 4,   p‑ERK↓, 1,   Gli1↓, 1,   miR-34a↑, 1,   Nanog↓, 1,   NOTCH1↓, 1,   p‑PI3K↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

miR-200c↑, 1,   MMPs↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumMeta↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,   OATPs↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CXCR4↓, 1,   IKKα↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABCG2↓, 7,   BioEnh↝, 1,   ChemoSen↑, 1,   CYP2C9↓, 1,   MRP1/ABCC1↓, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EZH2↓, 1,   Myc↓, 1,  
Total Targets: 49

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2/PTGS2↓, 1,   Inflam?, 1,  
Total Targets: 3

Scientific Paper Hit Count for: ABCG2, BCRP/ATP-binding cassette sub-family G member 2
1 Chrysin
1 Diclofenac
1 Garcinol
1 Isoliquiritigenin
1 Isovitexin
1 Quercetin
1 Aflavin-3,3′-digallate
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#:900  State#:%  Dir#:1
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