ABCG2 Cancer Research Results

ABCG2, BCRP/ATP-binding cassette sub-family G member 2: Click to Expand ⟱

Source:

Type:

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,

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,

*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

significantly suppressed the stem-like properties

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,

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.

8030-

IVM,

Metabolism and interactions of Ivermectin with human cytochrome P450 enzymes and drug transporters, possible adverse and toxic effects

Review,

Var,

P450↓, Ivermectin (IVM) as substrate and inhibitor of human P450 (P450, CYP) enzymes and drug transporters.
P-gp/ABCB1↓, . IVM exerts a potent inhibition of P-gp (ABCB1), MRP1 (ABCC1), MRP2 (ABCC2), and BCRP1 (ABCG2), a
ABCC2↓,
ABCG2↓,
OATPs↓, medium to weak inhibition of OATP1B1 (SLC21A6) and OATP1B3 (SLCOB3) transport activity

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.

8235-

LCA,

Anticancer effects of licochalcones: A review of the mechanisms

Review,

Var,

mt-Apoptosis↑, licochalcones can activate the mitochondrial apoptosis pathway and the death receptor pathway, promote autophagy-related protein expression, inhibit cell cycle protein expression,
TumAuto↑,
TumCMig↓, regulate cancer migration-related protein expression via multiple signaling pathways, including EGFR/ERK, PI3K/Akt/mTOR, p38/JNK, JAK2/STAT3, MEK/ERK, Wnt/β-catenin, and MKK4/JNK signaling pathways.
LC3‑Ⅱ/LC3‑Ⅰ↑, increasing the LC3-II/LC3-I ratio, as well as the levels of the autophagy-related proteins ATG5, ATG7, and P62.
ATG5↑,
ATG7↑,
p62↑,
CHOP/DDIT3↑, LA-induced increases in CHOP expression also promote autophagy
ER Stress↑, LA-induced autophagy in lung cancer cells is associated with the induction of endoplasmic reticulum stress
UPR↑, LA (10 μM) enhances the expression of miR-144-3p, causes unfolded protein response,
ATG3↑, triggers autophagy by promoting the accumulation and expression of ATG1, ATG3, ATG6, and ATG16 via activation of the PERK/ATF4/CHOP signaling pathway
Beclin-1/ATG6↑,
ATG16L1↑,
PERK↑,
ATF4↑,
ATP↓, LA (2.5–25 μM) inhibited ATP production and caused mitochondrial dysfunction in H1299 and H322 lung cancer cells by inhibiting hypoxia-induced HIF-1α accumulation and the expression of target genes GLUT1 and PDK1
Hif1a↓,
GLUT1↓,
PDK1 / PDPK1↓,
Bcl-xL↓, induce apoptosis in H460 and A549 lung cancer cells by decreasing the levels of Bcl-xL and Bcl-2 while increasing the levels of Bad, Bax, cleaved PARP, and caspase-3
Bcl-2↓,
BAD↑,
BAX↑,
Casp3↑,
survivin↓, LA (5–50 μM) downregulated the expression of survivin by inhibiting the EGFR signaling pathway and its downstream kinases ERK1/2 and AKT in H3255, HCC827, H1975, and A549 lung cancer cells
EGFR↓,
ERK↓,
Akt↓,
mtDam↑, LB (5–15 μM) inhibited the EGFR and MET signaling pathways and induced mitochondrial dysfunction and endoplasmic reticulum stress in HCC827 lung cancer cells, which induced the loss of MMP, release of cytochrome c, and increased expression of casp
MMP↓,
Cyt‑c↑,
Casp↑,
MDM2↓, By inhibiting the expression of MDM2, cyclin B1, CDC2, and CDC25C, LA (10–15 μM) led to cell cycle arrest of H460 and A549 lung cancer cells at the G2/M phase
CycB/CCNB1↓,
CDC2↓,
CDC25↓,
TumCCA↑,
TumCP↓, decreases in the proliferation of lung cancer cells by LA were related to the inhibition of the Wnt/β-catenin signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
Sp1/3/4↓, LA (2–20 μM) inhibited the AKT signaling pathway and the expression of the downstream transcription factor Sp1, which reduced the levels of MMP-1 and MMP-3 and inhibited the migration and invasion of A549 and H460 lung cancer cells
MMP-10↓,
MMP3↓,
TumCI↓,
Imm↑, Activation of the immune system
PD-L1↓, LA (10–50 μM) inhibited the expression of PD-L1 and thereby induced the production of reactive oxygen species (ROS) in A549 lung cancer cells, which inhibited the phosphorylation of 4EBP1, activated the PERK/eIF2α pathway,
ROS↑,
4E-BP1↓,
eIF2α↓,
PI3K↓, By inhibiting the PI3K/Akt/mTOR signaling pathway, LA (5–20 μM) activated the mitochondrial apoptosis pathway
mTOR↓,
p‑cMET↑, LA (1–50 μM) induced endoplasmic reticulum stress in HepG2 cells by inducing phosphorylation of VEGFR2, c-Met receptor, and PLCγ1 and enhancing the cytosolic Ca2+ release from the endoplasmic reticulum, which subsequently induced ROS accumulation
Ca+2↑,
RUBCN↓, LA-induced (5–50 μM) downregulation of PDK1 and rubicon by activating the ULK1/Atg13 signaling pathway and increasing the expression of TSC1/2, PRAS40, CTMP, and PP2A.
ATG13↑,
TSC1↑,
TSC2↑,
PRAS40↑,
PP2A↑,
ULK1/ATG1↑,
THEM4/CTMP↑,
DR5↑, LA activates the death receptor pathway and caspase cascade by increasing the expression of DR3, DR5, and Fas.
Fas↑,
TNFRSF25/DR3/APO3/LARD/TRAMP/WSL1↑,
PKCδ↓, LA also decreases the expression of the survival factor PKCε, p70S6K, and Akt.
P70S6K↓,
VEGF↓, Via downregulation of VEGF-A, LE (7–14 mg/kg) inhibited angiogenesis in cancer tissue in a xenograft mouse model using MDA-MB 231 breast cancer cells
angioG↓,
HK2↓, Moreover, the inhibitory effect of LA (10–50 μM) on the AKT signaling pathway can downregulate the expression of hexokinase 2A and inhibit glycolysis, thereby inducing apoptosis of MKN45 and SGC7901 cells
Glycolysis↓,
TrxR1↓, LA (10–40 μM) can enhance the production of intracellular ROS by inhibiting the expression of thioredoxin reductase-1, which activates the mitochondrial apoptosis pathway and induces apoptosis in HCT-116 cells
APAF1↑, By increasing intracellular Ca2+ and ROS levels, decreasing mitochondrial membrane potential, upregulating Apaf-1, caspase-9, caspase-3, and cleaved PARP levels, and elevating the Bax/Bcl-2 ratio, LA (10–80 μM) induced T24 cells apoptosis
cl‑PARP↑,
Bax:Bcl2↑,
ABCG2↓, By reducing the expression of BCRP, LA (10–100 μM) reduced the BCRP-mediated efflux of doxorubicin and temozolomide in BCRP-MDCKII cells.
BioEnh↑, Inhibition of BCRP expression can promote increased intestinal (re)uptake of antineoplastic drugs and decrease their hepatic metabolization, thereby enhancing their bioavailability.

8237-

LCA,

Role of Licochalcone A in Potential Pharmacological Therapy: A Review

Review,

Var,

*other↝, Licorice always functions as an adjuvant drug in traditional Chinese medicine to reduce the toxicity of other medicinal herbs or enhance their pharmacological effects.
*Inflam↓, LA demonstrates various pharmacological properties, including anti-inflammation, antibacterial, antioxidant, anti-parasitic, bone protection, neuroprotection, skin protection, and blood glucose and lipid regulation.
*Bacteria↓,
*antiOx↑,
*AntiP↑,
*neuroP↑,
*glucose↝,
*lipid-P↓,
PKCδ↓, Downregulation of PKCε, p70S6K, and Akt is also described
P70S6K↓,
Akt↓,
ER Stress↑, LA induced ER stress in HepG2 cells to induce apoptosis
Apoptosis↑,
Ca+2↑, enhancing cytosolic Ca2+ release from the ER
PI3K↓, apoptosis of MCF-7 by inhibiting PI3K-Akt-mTOR signaling, thereby increasing caspase-3 activity, decreasing expression of B-cell lymphoma-2, and triggering the release of cytochrome from mitochondria into the cytoplasm
mTOR↓,
Casp3↑,
Bcl-2↓,
Cyt‑c↑,
BAX↑, upregulation of Bax expression and PARP cleavage, downregulation of Bcl-2 and Cyclin D1, and accumulation of reactive oxygen species (ROS)
cl‑PARP↑,
cycD1/CCND1↑,
ROS↑,
CHOP/DDIT3↑, CHOP expression was elevated in parallel
ERK↑, LA significantly activated ERK and p38 in A549 and H460 cells in a time-dependent manner.
p38↑,
JNK↓, LA also inhibited the activity of JNK, suppressed the expression of c-IAP1, c-IAP2, XIAP, Survivin, c-FLIPL, and RIP1, and attenuated LA-induced induction of autophagy
IAP1↓,
XIAP↓,
survivin↓,
cFLIP↓,
RIP1↓,
EGFR↓, promoted the degradation of EGFR, Met, Her2
MET↓,
HER2/EBBR2↓,
p‑4E-BP1↓, LA may inhibit the phosphorylation of 4EBP1 (Ser 65) and activate the PERK-eIF2α pathway to inhibit PD-L1 translation
PERK↑,
eIF2α↑,
PD-L1↓,
HK2↓, Hexokinase 2Â (HK2) expression was downregulated at a lower dose, attenuating glycolysis elevation and inducing apoptosis in MKN-45 and SGC7901 cells
Glycolysis↓,
Sp1/3/4↓, LA induced apoptosis via downregulating the expression of specificity protein 1 (Sp1), upregulating Bax, Bid, Bcl-xl, caspase-3, and PARP cleavage with doses of 10–40 μM
FasL↑, LA induced apoptosis in KB cells, relying on activation of caspase-dependent factor associated suicide ligand (FasL) mediated death receptor pathway.
MMP↓, reducing mitochondrial membrane potential and inhibiting ATP production in vitro
ATP↓,
TumAuto↑, The literature also showed that LA induced apoptosis and autophagy in SiHa
WEE1↑, LA blocked the cell cycle in HepG2 cells by increasing the expression of Weel, P21, Cyclin D1, and JNK1 and decreasing the expression of Survivin, Cyclin B1, and CDK1 using doses of 30–70 μM
P21↑,
CDK1↓,
TumCCA↑,
TumCMig↓, LA exhibited the ability to inhibit migration and invasion of A549 and H460 cells at relatively lower doses (2–20 μM)
TumCI↓,
ABCG2↓, downregulating the expression of breast cancer resistance protein (BCRP)
HSP90↓, LA also reduced Hsp90 activity in gefitinib-resistant NSCLC cells (H1975) via binding to the N-terminal ATP binding site of Hsp90 to reduce drug resistance
T-Cell↑, LA (40 mg/kg) to C3H/HeN mice bearing UM-UC-3 cells enhanced the activity of cytotoxic T lymphocytes and counts of CD4+ CD25+ Foxp3+ T regulatory T cells. Thus, LA might treat bladder cancer by modulating the tumor immune microenvironment
CD4+↑,
CD25+↑,
FOXP3↑,
Imm↝,
*Inflam↓, LA demonstrates anti-inflammatory activity via interaction with MAPK, NF-κB, NLRP3, and Nrf2 signaling in the acute lung, kidney, and liver injury (acute inflammation) and arthritis and asthma
*NF-kB↓,
*NRF2↑,
*AntiArt↑,

8190-

LGE,

doxoR,

Cymbopogon citratus and Citral Overcome Doxorubicin Resistance in Cancer Cells via Modulating the Drug's Metabolism, Toxicity, and Multidrug Transporters

in-vitro,

BC,

MCF7

in-vitro,

Liver,

HepG2

in-vitro,

Ovarian,

SKOV3

ChemoSen↑, LG and citral (20 μg/mL) synergistically increased DOX cytotoxicity and lowered DOX dosage by >3-fold and >1.5-fold, respectively.
CYP3A4↓, LG and citral targeted metabolic molecules in resistant cells and significantly downregulated PXR, CYP3A4, GST, MDR1, MRP1, and PCRP genes.
PXR, NR1I2↓,
GSTA1↓,
MDR1↓,
MRP1/ABCC1↓,
ABCG2↓,

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

 40 uM

in-vitro,

Pca,

LNCaP

 LNCap and ARPE-19 cells

in-vitro,

Pca,

ARPE-19

  LNCap and ARPE-19 cells

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↓,

7951-

RT,

BuckWS,

The anticancer potential of the dietary polyphenol rutin: Current status, challenges, and perspectives

Review,

Nor,

*Dose↝, Though rutin is widely distributed in plants, buckwheat is considered as its major source
*BioAv↓, Rutin is not easily absorbed into the blood, since its sugar moiety blocks its passage through the intestinal epithelial layers, indicating its poor bioavailability compared to other flavonoid glycosides
*BioAv↓, several in vitro studies have reported the biodegradation of rutin by both intestinal and non-intestinal microorganisms including Pediococcus Q-05 (Kim et al. 1998), Cunninghamella echinulata ATCC 9244 (Araujo et al. 2013),
*BioAv↓, P-glycoprotein (P-gp) and multidrug resistance protein 1 (MRP1) located in the intestine expelled rutin out of the cell thereby negatively affect its absorption and decrease its bioavailability (Zhang et al. 2013). This explains the significant role
*BioAv↓, The results showed that rutin was recovered as glucuronides and/or sulfates of quercetin and as unconjugated quercetin aglycone, but no free rutin was found in plasma, corroborating the pharmacokinetic studies of rutin in rats
*BioAv↝, All these studies strongly suggest that quercetin glucuronide is the major metabolite formed and circulated in blood after the intake of rutin.
TumCP↓, Rutin has been shown to hinder the proliferation of diverse cancer cell types in vitro, including breast, glioma, pancreas, colon, liver, lung, skin, prostate, cervical, and ovarian cancer cells
Risk↓, Rutin has been reported to prevent different types of cancers in vivo, such as breast, colon, melanoma, prostate, lymphoma, and leukemia.
*radioP↑, Recent reports showed that rutin has protective effects against radiation-induced inflammation and prevents radiation-induced skin carcinogenesis.
chemoPv↑, Overall, rutin exhibits outstanding chemopreventive and radioprotective effects both in vitro and in vivo,
TumCCA↑, Rutin has been reported to arrest cell cycle progression in cancer cells. Rutin can inhibit cell cycle at different checkpoints, such as G1, G2/M, and S phases.
GSK‐3β↑, Rutin can induce apoptosis in A549 lung cancer cells by upregulating the expression of GSK 3b, a downstream regulator of Wnt/b-catenin signaling
Wnt↓,
β-catenin/ZEB1↓,
ROS↑, Figure 3
BAX↑,
Casp3↑,
Casp8↑,
Casp9↑,
PARP↑,
Beclin-1/ATG6↑,
ATG5↑,
LC3II↑,
DNMT1↓,
P21↑,
CDK1↑,
CycB/CCNB1↓,
TNF-α↑,
VEGF↓,
IL1β↓,
NF-kB↓,
AP-1↓,
MYCN↓,
AMPK↑,
MAPK↓,
PI3K↓,
Akt↓,
cMET↓,
P-gp/ABCB1↓,
MRP1/ABCC1↓,
ABCG2↓,
MMPs↓,
TNF-α↓,
iNOS↓,
COX2/PTGS2↓,
angioG↓, Moreover, administration of 200 mM/kg rutin can inhibit angiogenesis in B16F-10 melanoma bearing C57BL/6 mice through the prevention of capillary formation
STAT3↓, rutin’s ability to prevent STAT3 activation mediated cancer development.
*chemoP↑, Several studies have reported that rutin can alleviate the toxicities induced by cisplatin, a platinum-based anticancer drug in experimental animal models
*ROS↓, The possible mechanisms by which rutin might exert its protective effects are ROS inhibition, suppression of MDA levels, and downregulation of p53, caspase-3, caspase-9, and JNK/TNF/p38 MAPK pathways
*MDA↓,
*P53↓,
*Casp3↓,
*Casp9↓,
*JNK↓,
*TNF-α↓,
*p38↓,
*MAPK↓,
GSH↓, GSH level in tumor cells was decreased after combined treatment with rutin, indicating that rutin sensitized cancer cells to cisplatin.
ChemoSen↑,
*hepatoP↑, rutin could inhibit cyclophosphamide-induced hepatocytotoxicity, probably through the upregulation of antioxidant enzyme activities and downregulation of serum toxicity markers.
*COX1↓, Rutin protected intestine from methotrexate, an antimetabolite used in cancer therapy, and induced lesions by inhibiting the expression of COX-1, COX-2, and 15-lipoxygenase
*COX2/PTGS2↓,
*15-LOX/ALOX15↓,
RenoP↑, rutin might protect the kidney from doxorubicin-induced nephrotoxicity, probably by up-regulation of the activity of antioxidant enzymes.
*toxicity↓, According to clinical trials, the safe dosage of rutin is 500 mg/day (Sharma et al. 2013). Rutin is nontoxic both acutely and chronically and no evidence of injury has been found due to rutin administration

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 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

15-LOX/ALOX15↓, 1, AntiArt↑, 1, AntiP↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1, lipid-P↓, 1, MDA↓, 1, NRF2↑, 1, ROS↓, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

glucose↝, 1,

Cell Death(tgid=5) ⓘ

Casp3↓, 1, Casp9↓, 1, JNK↓, 1, MAPK↓, 1, p38↓, 1,

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 2, COX2/PTGS2↓, 2, Inflam?, 1, Inflam↓, 2, NF-kB↓, 1, TNF-α↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4, BioAv↝, 1, Dose↝, 1,

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1, hepatoP↑, 1, neuroP↑, 1, radioP↑, 1, toxicity↓, 1,

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,
Total Targets: 31

Scientific Paper Hit Count for: ABCG2, BCRP/ATP-binding cassette sub-family G member 2

2 Licochalcone A
1 Chrysin
1 Diclofenac
1 Garcinol
1 Isoliquiritigenin
1 Ivermectin
1 Isovitexin
1 Lemongrass Extract/Citral
1 doxorubicin
1 Quercetin
1 Rutin
1 buckwheat sprouts
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
  wNotes=on  sortOrder:rid,rpid

ABCG2 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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