MRP1/ABCC1 Cancer Research Results

MRP1/ABCC1, Multidrug Resistance Protein 1: Click to Expand ⟱
Source:
Type:
Multidrug resistance protein 1 (MRP1) encoded by ABCC1 gene.
MRP1 levels are elevated in numerous cancer types, NSCLC, breast cancer, and prostate cancer Multidrug Resistance Protein 1 (MDR1), also known as P-glycoprotein (P-gp) or ABCB1, is a membrane protein that functions as an efflux pump, transporting a variety of drugs and xenobiotics out of cells. Its expression is a significant factor in the development of multidrug resistance (MDR) in cancer therapy.

Resistance Protein 1 (MDR1) is often upregulated in various cancers, and its high expression is associated with poor prognosis and protumorigenic effects due to its role in drug resistance.
Field Suggested Entry
Target ABCC1 / MRP1
Full Name ATP-binding cassette subfamily C member 1 / multidrug resistance-associated protein 1
Target Class ATP-dependent ABC efflux transporter
Primary Biology Efflux of drugs, xenobiotics, organic anions, glutathione conjugates, oxidized glutathione, and inflammatory lipid mediators
Cancer Relevance High: contributes to multidrug resistance by exporting anticancer drugs and reducing intracellular drug accumulation
AD Relevance Medium: possible role in amyloid-β clearance and barrier transporter function, but less established than ABCB1/P-gp and LRP1
Therapeutic Direction Context-dependent. In cancer, inhibition/down-modulation may improve chemotherapy retention in tumor cells. In AD, support/upregulation may be desirable if enhancing amyloid-β clearance. Systemic inhibition may increase normal-tissue toxicity.


Scientific Papers found: Click to Expand⟱
5248- Ba,  BA,  doxoR,    Baicalin and Baicalein Enhance Cytotoxicity, Proapoptotic Activity, and Genotoxicity of Doxorubicin and Docetaxel in MCF-7 Breast Cancer Cells
- in-vitro, BC, MCF7 - in-vitro, Nor, HUVECs
toxicity↝, We have found that baicalin and baicalein demonstrated cytotoxicity towards both cell lines, with more potent effects observed in baicalein.
ChemoSen↑, Both flavonoids, baicalin (167 µmol/L) and baicalein (95 µmol/L), synergistically enhanced the cytotoxic, proapoptotic, and genotoxic activity of doxorubicin and docetaxel in breast cancer cells.
selectivity↑, Surprisingly, low concentrations of baicalin and baicalein had a greater effect on MCF-7 viability. A
Apoptosis↑, Induction of Apoptosis and Necrosis by Baicalin and Baicalein Used alone and in Combination with Anticancer Drugs
necrosis↑,
MMP↓, After treatment with baicalin and baicalein at high concentrations (IC50), the ΔΨm of cancer cells was diminished to 30% of the control value
DNAdam↑, DNA Damage Induced by Baicalin and Baicalein Used Alone and in Combination with Anticancer Drugs
cl‑PARP↑, PARP Cleavage Induced by Baicalin and Baicalein Used Alone and in Combination with Anticancer Drugs
MRP1/ABCC1↓, Moreover, baicalin and baicalein reduced cisplatin resistance by inhibiting the expression of genes involved in drug resistance, such as MRP1 [30] and Bcl-2, and via the Akt/mTOR and Nrf2/Keap 1 pathway [26].
Bcl-2↓,
hepatoP↑, baicalin and baicalein can also help decrease the side effects of cisplatin treatment by protecting the liver from damage [31]
cardioP↑, Similar to baicalein, baicalin also significantly protects against doxorubicin’s cardiotoxicity.
BioAv↝, This is because baicalein has a smaller size and high lipophilicity, contributing to fast absorption and an improved ability to penetrate cells [60].

6503- BCP,    The Potential Therapeutic Role of Beta-Caryophyllene as a Chemosensitizer and an Inhibitor of Angiogenesis in Cancer
- Review, Var, NA
ChemoSen↑, Beta-Caryophyllene (BCP), was highlighted in several recent preclinical studies to enhance chemo-sensitization in chemo-resistant tumors and to efficiently inhibit angiogenesis and cancer cells’ ability to invade and metastasize.
angioG↓,
TumCI↓,
TumMeta↓,
ROS↑, BCP seems to work as a dual modulator of oxidative stress, increasing reactive oxygen species (ROS) in cancer cells, and thus enhancing apoptosis, but reducing ROS in normal cells to protect them from damage
*ROS↓,
chemoP↑,
CB2 / CNR2↑, important issue in BCP is its ability to bind to the body’s cannabinoid receptor 2 (CB2), where it binds selectively to the CB2 receptors and not the CB1 receptor, which makes it non-psychoactive and therapeutically appealing.
Inflam↓, activation of the CB2 receptor by BCP can suppress pro-inflammatory cytokines production, helping to create an anti-tumor immune environment
AntiTum↑,
*BioAv↑, Beta-Caryophyllene, a food additive approved by the Food and Drug Administration, is efficiently absorbed in the gastro-intestinal tract and can penetrate the blood–brain barrier and has a well-established safety profile, making it an attractive biom
*BBB↑,
Apoptosis↑, Induces apoptosis and suppresses proliferative activity of lung cancer cells
TumCP↑,
TumCCA↑, Induces G1 cell cycle arrest by dysregulating cyclins and other molecules
RadioS↑, GBM: Works as a potential radiosensitizer for improving RT outcomes by inhibiting DNA repair, inducing apoptosis, and suppressing anti-apoptotic and survival pathways
DNArepair↓,
ROS↑, BC: Enhances sensitization and promotes the cigarette smoke condensate (CSC)-induced apoptosis in MDA-MB-468 cells, mainly by triggering oxidative stress and inhibition of STAT3
STAT3↓,
*BioEnh↑, BCP is considered a key component in black pepper’s ability to enhance nutrient absorption, including compounds like curcumin.
Pain↓, BCP in cloves further supports their role in pain management and infection prevention.
AntiBio↓,
ROS↑, selectively induce apoptosis and oxidative stress in cancer cells while sparing normal cells at lower concentrations.
Dose↝, I50, for many cancer cell lines typically ranges from 19 to 64 μM
NF-kB↓, Beta-Caryophyllene was reported to inhibit the central to the regulators of inflammation, NF-κB and MAPK pathways, leading to a decrease in pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) production
MAPK↓,
TNF-α↓,
IL1β↓,
IL6↓,
cl‑PARP↑, through increasing the levels of cleaved PARP, caspases and Bax, and the downregulation of Bcl-2, directly by interaction with CB2.
Casp↑,
BAX↑,
Bcl-2↓,
VEGF↓, BCP blocks migration of endothelial cells by inhibiting the secretion of VEGF, and thus blocking the activity of the tyrosine kinase VEGFR2
VEGFR2↓,
MMP2↓, BCP can also prohibit the secretion of MMP-2, p-p38 and p-ERK
p‑p38↓,
p‑ERK↓,
EPR↑, BCP was suggested to accumulate in the cancer cell membrane, altering the cells’ permeability, leading to the accumulation of anticancer drugs, and consequently strengthening the drugs’ activity.
P-gp↓, direct inhibition of P-glycoprotein (P-gp/ABCB1) and multidrug resistance-associated protein 1 (MRP1/ABCC1), which are overexpressed in resistant tumors
MRP1/ABCC1↓,
*NRF2↑, Importantly, BCP’s selective antioxidant activity—activating Nrf2 in normal cells while increasing ROS in cancer cells—minimizes off-target toxicity,
*antiOx↑,

5690- BJ,  BRU,    Brusatol: A potential sensitizing agent for cancer therapy from Brucea javanica
- Review, Var, NA
NRF2↓, Brusatol is a potent Nrf2 inhibitor for future cancer treatment.
TumCG↓, Brusatol exhibits significant tumor inhibition in multiple cancers.
ChemoSen↑, also exhibits significant synergistic antitumor effects in combination with chemotherapeutic agents
ROS↑, Graphical Abstract
NF-kB↓,
Akt↓,
mTOR↓,
TumCCA↑,
Apoptosis↑,
PARP↑,
Casp↑,
P53↓,
Bcl-2↓,
PI3K↓,
JAK2↓,
EMT↓,
p27↑,
ROCK1↓,
MMP2↓,
MMP9↓,
NRF2↓, which is the reason why brusatol is called an Nrf2 inhibitor [15]. Brusatol is a potent Nrf2 inhibitor
AntiTum↑, Brusatol shows significant antitumor effects in vitro and in vivo
HO-1↓, Moreover, brusatol inhibited the expression of Nrf2 downstream genes, such as HO-1 [19], [31], [32], NQO1 [43], [44], VEGF [45], and AKR1C1 [46].
NQO1↓,
VEGF↓,
MRP1/ABCC1↓, brusatol reduced both the mRNA and protein levels of NQO1, HO-1, MDR1, and MRP5
RadioS↑, Improvement of sensitivity to radiotherapy and phototherapy
PhotoS↑,
toxicity↝, the toxicity of brusatol is a problem that can not be ignored.

5649- BNL,    Borneol, a novel agent that improves central nervous system drug delivery by enhancing blood–brain barrier permeability
- Review, Nor, NA
*BBB↑, A growing body of evidence confirms that the ‘orifice-opening’ effect of borneol is principally derived from opening the BBB. Borneol is therefore believed to be an effective adjuvant that can improve drug delivery to the brain
*other↑, Borneol also protects the structural integrity of the BBB against pathological damage.
*P-gp↓, Both in vitro and in vivo studies have shown that borneol inhibited the expression of P-gp and other ABC transporters,
*toxicity⇅, Natural borneol has been extensively used in aromatherapy and in natural and cosmetic products because of its low toxicity compared to synthetic borneol, which toxicity is relatively high as it degrades slowly during storage, and noxious camphor
*BioAv⇅, In mice, a single oral dose of borneol accumulates in organs in the order of liver > brain > kidney > heart > spleen > muscle > lung, which confirms its considerably higher bioavailability in the brain than in most other organs
*Dose↑, Intranasal drug delivery can avoid gastrointestinal destruction and hepatic first-pass metabolism, resulting in rapid onset of effect and high brain bioavailability.
*ABC↓, Both in vitro and in vivo studies have shown that borneol inhibited the expression of P-gp and other ABC transporters,
*MRP1/ABCC1↓, including multidrug resistance protein 1 (Mrp1), 1a (Mdr1a) and 1 b (Mdr1b),
*5HT↑, systemic borneol was found to increase the levels of histamine and serotonin in the hypothalamus
*GABA↑, and levels of l-aspartic acid, glutamate, glycine and γ-aminobutyric acid (GABA) in the corpus striatum of rats (Zhang et al., 2012).
*eff↑, Co-incubation with borneol increased the uptake of Huperzine A loaded aprotinin-modified nanoparticles by capillary endothelial cells

5695- BRU,    Brusatol enhances the efficacy of chemotherapy by inhibiting the Nrf2-mediated defense mechanism
- in-vitro, Lung, A549
NRF2↓, Here, we report the identification of brusatol as a unique inhibitor of the Nrf2 pathway that sensitizes a broad spectrum of cancer cells and A549 xenografts to cisplatin and other chemotherapeutic drugs.
ChemoSen↑,
Apoptosis↑, induced apoptosis, reduced cell proliferation, and inhibited tumor growth more substantially when compared with cisplatin treatment alone.
TumCP↓,
TumCG↓,
MRP1/ABCC1↓, the protein level of Nrf2-target genes, including γGCS, MRP1, and MRP2, was also reduced in a dose-dependent manner, whereas only a slight reduction in NQO1 was observed
GSH↓, Brusatol Treatment Decreased Glutathione Levels and Increased the Intracellular Concentration of Cisplatin.
cMyc↓, inhibition of both Nrf2 and c-Myc by brusatol

5965- CEL,  Cisplatin,    Celecoxib enhances anticancer effect of cisplatin and induces anoikis in osteosarcoma via PI3K/Akt pathway
- in-vitro, OS, MG63
COX2↓, celecoxib, a cyclooxygenase-2 inhibitor, induces apoptosis in human osteosarcoma cell line MG-63 via down-regulation of PI3K/Akt.
ChemoSen↑, It has been confirmed that celecoxib enhances apoptosis and cytotoxic effect of cisplatin
MDR1↓, MDR1, MRP1, BCRP and Trkb, E-cadherin, β-catenin were significantly downregulated in cells treated with the combination of celecoxib and cisplatin
MRP1/ABCC1↓,
E-cadherin↓,
β-catenin/ZEB1↓,
Apoptosis↑, Down-regulation of MDR1, MRP1 and BCRP correlated with increased apoptosis
TumCCA↑, celecoxib caused G1 phase arrest and significantly inhibited cell growth,
TumCG↓,
P-gp↓, COX-inhibitors may sensitize cancer cells to chemotherapeutic drugs via inhibiting P-gp, MRP1 and BCRP, and enhance the effect of anticancer drugs
PI3K↓, COX-2 inhibitors are known to inhibit the PI3K/Akt pathway
Akt↓,

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↓,
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↓,

2946- PL,    Piperlongumine, a potent anticancer phytotherapeutic: Perspectives on contemporary status and future possibilities as an anticancer agent
- Review, Var, NA
ROS↑, piperlongumine inhibits cancer growth by resulting in the accumulation of intracellular reactive oxygen species, decreasing glutathione and chromosomal damage, or modulating key regulatory proteins, including PI3K, AKT, mTOR, NF-kβ, STATs, and cycD
GSH↓, reduced glutathione (GSH) levels in mouse colon cancer cells
DNAdam↑,
ChemoSen↑, combined treatment with piperlongumine potentiates the anticancer activity of conventional chemotherapeutics and overcomes resistance to chemo- and radio- therapy
RadioS↑, piperlongumine treatment enhances ROS production via decreasing GSH levels and causing thioredoxin reductase inhibition
BioEnh↑, Moreover, the bioavailability is significantly improved after oral administration of piperlongumine
selectivity↑, It shows selectivity toward human cancer cells over normal cells and has minimal side effects
BioAv↓, ts low aqueous solubility affects its anti-cancer activity by limiting its bioavailability during oral administration
eff↑, encapsulation of piperlongumine in another biocompatible natural polymer, chitosan, has been found to result in pH-dependent piperlongumine release and to enhance cytotoxicity via efficient intracellular ROS accumulation against human gastric carcin
p‑Akt↓, Fig 2
mTOR↓,
GSK‐3β↓,
β-catenin/ZEB1↓,
HK2↓, iperlongumine treatment decreases cell proliferation, single-cell colony-formation ability, and HK2-mediated glycolysis in NSCLC cells via inhibiting the interaction between HK2 and voltage-dependent anion channel 1 (VDAC1)
Glycolysis↓,
Cyt‑c↑,
Casp9↑,
Casp3↑,
Casp7↑,
cl‑PARP↑,
TrxR↓, piperlongumine (4 or 12 mg/kg/day for 15 days) administration significantly inhibits increase in tumor weight and volume with less TrxR1 activity in SGC-7901 cell
ER Stress↑,
ATF4↝,
CHOP↑, activating the downstream ER-MAPK-C/EBP homologous protein (CHOP) signaling pathway
Prx4↑, piperlongumine kills high-grade glioma cells via oxidative inactivation of PRDX4 mediated ROS induction, thereby inducing intracellular ER stress
NF-kB↓, piperlongumine treatment (2.5–5 mg/ kg body weight) decreases the growth of lung tumors via inhibition of NF-κB
cycD1/CCND1↓, decreases expression of cyclin D1, cyclin- dependent kinase (CDK)-4, CDK-6, p- retinoblastoma (p-Rb)
CDK4↓,
CDK6↓,
p‑RB1↓,
RAS↓, piperlongumine downregulates the expression of Ras protein
cMyc↓, inhibiting the activity of other related proteins, such as Akt/NF-κB, c-Myc, and cyclin D1 in DMH + DSS induced colon tumor cells
TumCCA↑, by arresting colon tumor cells in the G2/M phase of the cell cycle
selectivity↑, hows more selective cytotoxicity against human breast cancer MCF-7 cells than human breast epithelial MCF-10A cells
STAT3↓, thus inducing inhibition of the STAT3 signaling pathway in multiple myeloma cells
NRF2↑, Nrf2) activation has been found to mediate the upregulation of heme oxygenase-1 (HO-1) in piperlongumine treated MCF-7 and MCF-10A cells
HO-1↑,
PTEN↑, stimulates ROS accumulation; p53, p27, and PTEN overexpression
P-gp↓, P-gp, MDR1, MRP1, survivin, p-Akt, NF-κB, and Twist downregulation;
MDR1↓,
MRP1/ABCC1↓,
survivin↓,
Twist↓,
AP-1↓, iperlongumine significantly suppresses the expression of transcription factors, such as AP-1, MYC, NF-κB, SP1, STAT1, STAT3, STAT6, and YY1.
Sp1/3/4↓,
STAT1↓,
STAT6↓,
SOX4↑, increased expression of p21, SOX4, and XBP in B-ALL cells
XBP-1↑,
P21↑,
eff↑, combined use of piperlongumine with cisplatin enhances the sensitivity toward cisplatin by inhibiting Akt phosphorylation
Inflam↓, inflammation (COX-2, IL6); invasion and metastasis, such as ICAM-1, MMP-9, CXCR-4, VEGF;
COX2↓,
IL6↓,
MMP9↓,
TumMeta↓,
TumCI↓,
ICAM-1↓,
CXCR4↓,
VEGF↓,
angioG↓,
Half-Life↝, The analysis of the plasma of piperlongumine treated mice (50 mg/kg) after intraperitoneal administration, 1511.9 ng/ml, 418.2 ng/ml, and 41.9 ng/ml concentrations ofplasma piperlongumine were found at 30 minutes, 3 hours, and 24 hours, respecti
BioAv↑, Moreover, the bioavailability is significantly improved after oral administration of piperlongumine

81- QC,  EGCG,    Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea
- in-vivo, Pca, NA
COMT↓,
MRP1/ABCC1↓,
Ki-67↓,
Bax:Bcl2↑,
AR↓, significant increase in the inhibition of proliferation, androgen receptor (AR) and phosphatidylinositol 3-kinases (PI3K)/Akt signaling, and stimulation of apoptosis.
Akt↓,
p‑ERK↓, ERK1/2
COMT↓, Increased inhibition of COMT protein and mRNA expression and MRP1 protein expression
eff↑, Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea
chemoPv↑, novel regimen by combining GT and Q to improve chemoprevention in a non-toxic manner and warrant future studies in humans.
BioAv↑, Increased bioavailability and decreased methylation of GTPs


Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

GSH↓, 2,   HO-1↓, 1,   HO-1↑, 1,   NQO1↓, 1,   NRF2↓, 3,   NRF2↑, 1,   Prx4↑, 1,   ROS↑, 5,   SOD2↓, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 2,   Glycolysis↓, 1,   HK2↓, 1,   LDHA↓, 1,   MCT4↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   p‑Akt↓, 1,   Apoptosis↑, 5,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Casp↑, 2,   Casp3↑, 1,   Casp7↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   MAPK↓, 1,   MDM2↓, 1,   Myc↓, 1,   necrosis↑, 1,   p27↑, 1,   p‑p38↓, 1,   survivin↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↓, 1,   PhotoS↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↑, 1,   ER Stress↑, 1,   XBP-1↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 2,   DNArepair↓, 1,   P53↓, 1,   PARP↑, 1,   cl‑PARP↑, 3,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   E2Fs↓, 1,   P21↑, 1,   p‑RB1↓, 1,   TumCCA↑, 4,  

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

EMT↓, 1,   p‑ERK↓, 2,   GSK‐3β↓, 1,   mTOR↓, 2,   PI3K↓, 2,   PTEN↑, 1,   RAS↓, 1,   STAT1↓, 1,   STAT3↓, 2,   STAT6↓, 1,   TumCG↓, 3,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   E-cadherin↓, 1,   Ki-67↓, 1,   MMP2↓, 2,   MMP9↓, 2,   ROCK1↓, 1,   SOX4↑, 1,   TumCI↓, 2,   TumCP↓, 1,   TumCP↑, 1,   TumMeta↓, 2,   Twist↓, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   ATF4↝, 1,   EPR↑, 1,   VEGF↓, 4,   VEGFR2↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,   P-gp↓, 3,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CB2 / CNR2↑, 1,   COX2↓, 2,   CXCR4↓, 1,   ICAM-1↓, 1,   IKKα↓, 1,   IL1β↓, 1,   IL6↓, 2,   Inflam↓, 2,   JAK2↓, 1,   NF-kB↓, 3,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,   CDK6↓, 1,   COMT↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABCG2↓, 1,   BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 1,   BioEnh↑, 1,   ChemoSen↑, 6,   Dose↝, 1,   eff↑, 3,   Half-Life↝, 1,   MDR1↓, 2,   MRP1/ABCC1↓, 8,   RadioS↑, 3,   selectivity↑, 3,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,   IL6↓, 2,   Ki-67↓, 1,   Myc↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 2,   cardioP↑, 1,   chemoP↑, 1,   chemoPv↑, 1,   hepatoP↑, 1,   Pain↓, 1,   toxicity↝, 2,  
Total Targets: 121

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   NRF2↑, 1,   ROS↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,   P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2↓, 1,   Inflam?, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   GABA↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABC↓, 1,   BioAv↑, 1,   BioAv⇅, 1,   BioEnh↑, 1,   Dose↑, 1,   eff↑, 1,   MRP1/ABCC1↓, 1,  

Functional Outcomes(tgid=23) ⓘ

toxicity⇅, 1,  
Total Targets: 19

Scientific Paper Hit Count for: MRP1/ABCC1, Multidrug Resistance Protein 1
2 brusatol
1 Baicalein
1 Baicalin
1 doxorubicin
1 Beta-Caryophyllene
1 Brucea javanica
1 borneol
1 Celecoxib
1 Cisplatin
1 Diclofenac
1 Piperlongumine
1 Quercetin
1 EGCG (Epigallocatechin Gallate)
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#:424  State#:%  Dir#:1
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