| 2001 |
MRP7/ABCC10 is a 1492 amino acid ABC transporter with three membrane-spanning domains (structural architecture resembling MRP1/2/3/6), confirmed by synthesis of an ~158 kDa protein in reticulocyte lysates programmed with the MRP7 cDNA, and maps to chromosome 6p12-21. |
cDNA sequence analysis, reticulocyte lysate in vitro translation, fluorescence in situ hybridization |
Cancer letters |
Medium |
11146224
|
| 2003 |
ABCC10/MRP7 mediates MgATP-dependent transport of the amphipathic anion 17β-estradiol-17β-D-glucuronide (E2 17βG) with Km ~57.8 µM and Vmax ~53.1 pmol/mg/min in membrane vesicles; LTC4 is a potent competitive inhibitor (Ki ~1.5 µM), and the pump shows modest LTC4 transport but not other canonical MRP substrates tested. |
Membrane vesicle transport assay using HEK293 cells transfected with MRP7 expression vector; competitive inhibition kinetics |
Molecular pharmacology |
High |
12527806
|
| 2004 |
ABCC10/MRP7 overexpression in HEK293 cells confers resistance to docetaxel (9–13-fold), paclitaxel (3-fold), vincristine (3-fold), and vinblastine (3–4-fold); MRP7-transfected cells show reduced accumulation of radiolabeled paclitaxel, consistent with ATP-dependent efflux pump activity. |
Ectopic expression in HEK293 cells, cytotoxicity assays, radiolabeled drug accumulation assay |
Cancer research |
High |
15256465
|
| 2009 |
ABCC10/MRP7 confers resistance to nucleoside analogues (cytarabine/Ara-C, gemcitabine, 2',3'-dideoxycytidine, PMEA) and epothilone B in addition to taxanes and vinca alkaloids; buthionine sulfoximine did not attenuate MRP7-conferred resistance, indicating MRP7-mediated transport does not involve glutathione (unlike MRP1/2). |
MRP7-transfected HEK293 cells and mouse embryo fibroblasts deficient in P-gp and Mrp1; cytotoxicity and radiolabeled drug accumulation assays |
Cancer research |
High |
19118001
|
| 2011 |
Abcc10 knockout mice show that Abcc10 is an endogenous resistance factor in vivo: Abcc10−/− mouse embryo fibroblasts are hypersensitive to docetaxel, paclitaxel, vincristine, and Ara-C with increased drug accumulation; Abcc10−/− mice treated with paclitaxel exhibit increased lethality with neutropenia and bone marrow/spleen/thymus toxicity. |
Abcc10−/− mouse generation, MEF cytotoxicity/accumulation assays, in vivo paclitaxel treatment with pathological assessment |
Cancer research |
High |
21576088
|
| 2012 |
ABCC10 substrates E2 17βG and LTC4 stimulate ABCC10 BeFx-sensitive ATPase activity; tamoxifen is identified as a novel substrate and ATPase stimulator; docetaxel, paclitaxel, and Ara-C also increase basal ATPase activity. ABCC10 localizes to the basolateral cell surface and exports docetaxel from apical to basolateral side in transepithelial LLC-PK1 assays. Sorafenib and cepharanthine inhibit ABCC10 docetaxel transport activity. |
Crude membrane ATPase assays with BeFx (vanadate-sensitive controls), transepithelial well assay in ABCC10-overexpressing LLC-PK1 cells, radiolabeled docetaxel transport |
Cancer research |
High |
23087055
|
| 2008 |
Sulfinpyrazone (an ABCC10 inhibitor) alters sensitivity to paclitaxel in ABCC10-expressing NSCLC cells concomitant with increased intracellular paclitaxel accumulation; siRNA knockdown of ABCC10 enhances paclitaxel cytotoxicity in NCI-H23 cells with increased intracellular paclitaxel, confirming ABCC10 effluxes paclitaxel endogenously in lung cancer cells. |
siRNA knockdown in NSCLC cells, pharmacological inhibition with sulfinpyrazone, intracellular paclitaxel accumulation assay |
Molecular cancer therapeutics |
Medium |
18445659
|
| 2009 |
Lapatinib and erlotinib (EGFR TKIs) reverse MRP7/ABCC10-mediated multidrug resistance by inhibiting drug efflux function (increased intracellular [3H]-paclitaxel accumulation and decreased efflux in MRP7-transfected cells) without altering MRP7 protein expression levels. |
MRP7-transfected HEK293 cells, cytotoxicity assay, [3H]-paclitaxel accumulation and efflux assays, Western blot |
Biochemical pharmacology |
Medium |
19720054
|
| 2009 |
Imatinib and nilotinib (BCR-Abl TKIs) reverse MRP7/ABCC10-mediated multidrug resistance by inhibiting paclitaxel efflux and increasing intracellular [3H]-paclitaxel accumulation in MRP7-transfected HEK293 cells, without altering MRP7 expression. |
MRP7-transfected HEK293 cells, MTT assay, [3H]-paclitaxel accumulation and efflux assays, Western blot |
PloS one |
Medium |
19841739
|
| 2008 |
Cepharanthine reverses MRP7/ABCC10-mediated paclitaxel resistance and competitively inhibits E2 17βG transport by MRP7 in membrane vesicle assays with a Ki of 4.86 µM, identifying it as a competitive inhibitor of ABCC10. |
MRP7-transfected HEK293 cells, paclitaxel accumulation/efflux assays, membrane vesicle E2 17βG transport competitive inhibition assay |
Biochemical pharmacology |
Medium |
19150344
|
| 2011 |
Tenofovir (TFV) is a substrate for ABCC10: TFV accumulation is 35% lower in HEK293-ABCC10 cells than parental HEK293 cells, reversed by cepharanthine; siRNA knockdown of ABCC10 increases TFV accumulation in CD4+ cells (18%) and monocyte-derived macrophages (25%). |
ABCC10-transfected HEK293 cells, pharmacological inhibition with cepharanthine, siRNA knockdown in primary CD4+ cells and macrophages, drug accumulation assay |
The Journal of infectious diseases |
Medium |
21628669
|
| 2012 |
Nevirapine is a substrate for ABCC10: accumulation is 37% lower in HEK293-ABCC10 cells vs. parental, reversed by cepharanthine; siRNA knockdown increases nevirapine accumulation in CD4+ cells (32%) and monocyte-derived macrophages (38%). |
ABCC10-transfected HEK293 cells, siRNA knockdown in CD4+ cells and macrophages, drug accumulation assays, pharmacological inhibition |
Pharmacogenetics and genomics |
Medium |
22082652
|
| 2017 |
FOXM1 promotes 5-FU resistance in colorectal cancer by directly binding to the ABCC10 promoter and driving its transcription; ABCC10 inhibition reverses FOXM1-induced 5-FU resistance in vivo. |
Chromatin immunoprecipitation (promoter binding), FOXM1 overexpression and silencing in CRC cells, in vivo xenograft with ABCC10 inhibitor |
Oncotarget |
Medium |
28051999
|
| 2018 |
ABCC10 actively effluxes gefitinib with an efflux ratio of 7.8 in an in vitro transport assay; overexpression of ABCC10 reduces intracellular gefitinib accumulation and decreases gefitinib sensitivity in NSCLC cells and xenograft models. |
In vitro transport assay, ABCC10-overexpressing cell lines, intracellular gefitinib accumulation measurement, in vivo xenograft |
Frontiers in pharmacology |
Medium |
30515095
|
| 2021 |
Exosomal delivery of the m6A demethylase FTO from gefitinib-resistant cells to recipient cells decreases m6A modification on ABCC10 mRNA, reducing YTHDF2-mediated decay and thereby increasing ABCC10 expression, which mediates gefitinib resistance transfer. |
Exosome internalization assays, m6A quantification, FTO knockdown/overexpression, YTHDF2 functional studies, in vitro and in vivo resistance models |
Molecular cancer research |
Medium |
33563765
|
| 2014 |
Abcc10 loss in MMTV-PyVmT mammary tumor mice results in faster tumor growth with reduced apoptosis and reduced metastasis; Abcc10-null tumor-derived cell lines are less migratory; Abcc10−/− mice show increased survival upon docetaxel treatment, confirming in vivo role as docetaxel resistance factor in mammary tumors. |
Abcc10−/− x MMTV-PyVmT mouse cross, allograft and cellular assays, migration assays, in vivo docetaxel treatment survival analysis |
British journal of cancer |
Medium |
24937672
|
| 2021 |
ABCC10 homology model (based on cryo-EM structure of MRP1) combined with molecular dynamics simulations and docking identifies predicted substrate- and modulator-binding sites within the transmembrane region of MRP7/ABCC10, with motion patterns consistent with the ABC efflux mechanism. |
Homology modeling based on MRP1 cryo-EM structure, molecular dynamics simulation, in silico docking |
MedComm |
Low |
34766143
|
| 2022 |
LXRα activation by its agonist TO901317 alters ABCC10 gene expression in rat hepatic and cardiac tissues, identifying ABCC10 as a specific LXRα target gene. |
In vivo rat hypercholesterolemia model, LXRα agonist treatment, hepatic/cardiac gene expression analysis |
Biochemical and biophysical research communications |
Low |
35462094
|
| 2023 |
ABCC10 redistributes from plasma membrane to lysosomes in paclitaxel-resistant cancer cells; lysosome-localized ABCC10 (along with ABCC3 and ABCC5) contributes to sequestration of doxorubicin and paclitaxel-OregonGreen488 in lysosomes; siRNA silencing of ABCC10 limits lysosomal drug accumulation. |
Western blot and confocal microscopy for localization, siRNA knockdown, ABCC inhibitors, flow cytometry for drug accumulation in lysosomes in paclitaxel-resistant TNBC and NSCLC cells |
Cellular physiology and biochemistry |
Medium |
37767694
|
| 2023 |
ABCC10 regulates glucosylceramide (GlcCer) synthesis and efflux differentially: sorafenib (ABCC10 inhibitor) decreases both GlcCer synthesis and efflux, while cepharanthine reduces only GlcCer efflux but not synthesis, in Huh-7 liver cells. |
Pharmacological inhibition with sorafenib and cepharanthine, GlcCer synthesis and efflux measurement in Huh-7 cells |
Nutrients |
Low |
36678216
|
| 2022 |
ABCC10 deletion in mice results in lower plasma and intestinal triglycerides (~38% and 36% reduction), ameliorates diet-induced obesity, reduces oleate uptake by enterocytes (~25–30%), and reduces intestinal triglyceride absorption (~37%), indicating ABCC10 regulates dietary fat absorption. |
Abcc10 knockout mice, plasma/intestinal lipid measurements, insulin/glucose tolerance tests, intestinal fat absorption assays |
International journal of molecular sciences |
Medium |
36430292
|
| 2025 |
ABCC10 binds and effluxes 2'3'-cyclic GMP-AMP (cGAMP) in an ATP-dependent manner at the R545 site; ABCC10-mediated cGAMP export suppresses the STING-TBK1-IRF3 signaling pathway, reducing RT-induced ROS and DNA damage, thereby conferring radiotherapy resistance. Nilotinib (ABCC10 inhibitor) combined with radiotherapy synergistically inhibits tumor growth in vivo. |
CRISPR metabolic library screen, vesicle transport assay, molecular docking, ELISA for cGAMP, RNA transcriptomics, ABCC10 overexpression and silencing, in vivo tumor radiotherapy + nilotinib combination |
Cell death and differentiation |
Medium |
40770563
|
| 2025 |
BRG1 (SMARCA4)-containing SWI/SNF chromatin remodeling complex enables transcription of ABCC10 (along with ABCC3 and ABCC5); pharmacological inhibition (PFI3) or PROTAC degradation (ACBI1) of SWI/SNF, or BRG1 siRNA silencing, substantially reduces ABCC10 transcription and reverses lysosomal drug sequestration in paclitaxel-resistant cancer cells. |
SMARCA4 siRNA knockdown, PFI3/ACBI1 pharmacological SWI/SNF inhibition, ABCC10 gene expression, lysosomal drug distribution in paclitaxel-resistant TNBC and NSCLC cells |
bioRxivpreprint |
Medium |
|