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BIOMARKER:

ABCG2 overexpression

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Other names: ABCG2, ABCP, BCRP, CD338, EST157481, MXR, ATP-binding cassette, sub-family G (WHITE), member 2 (Junior blood group)
Entrez ID:
Related biomarkers:
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Trials
3ms
Quinacrine and Curcumin in combination decreased the breast cancer angiogenesis by modulating ABCG2 via VEGF A. (PubMed, J Cell Commun Signal)
An induction of vascularization was noticed in PDX mice but reduction of vascularization was also observed after treatment of Cur + QC. Thus, data suggested that in hypoxia, ABCG2 enhances the production of angiogenesis factor VEGF A which in turn induced angiogenesis and Cur + QC inhibited the process by inhibiting ABCG2 in breast cancer.
Journal
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VEGFA (Vascular endothelial growth factor A) • ABCG2 • NOS3 (Nitric oxide synthase 3)
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ABCG2 overexpression • ABCG2 expression
11ms
Establishment and characterization of a topotecan resistant lung cancer NCI H460/TPT10 cell line and a tumor xenograft model (AACR 2022)
NCI-H460/TPT10 cells exhibited a 394.7-fold resistance to TPT, and cross-resistance to SN-38, mitoxantrone, and doxorubicin, compared to parental NCI-H460 cells...Moreover, the involvement of functional ABCG2 as a drug efflux pump conferring multidrug resistance (MDR) was indicated by low intracellular accumulation of TPT in NCI-H460/TPT10 cells, and the reversal effects by ABCG2 inhibitor Ko143 and cabozantinib. The NCI-H460/TPT10 and its parental cell line were further used to establish in vivo tumor xenograft mouse models, which verified their capability to serve as clinically relevant models for drug screening and the development of targeted strategies to overcome ABCG2-mediated MDR in NSCLC.
Preclinical
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ABCB1 (ATP Binding Cassette Subfamily B Member 1) • ABCG2 • ABCC1 (ATP Binding Cassette Subfamily C Member 1)
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ABCG2 overexpression • ABCG2 expression
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Cabometyx (cabozantinib tablet) • doxorubicin hydrochloride • topotecan • mitoxantrone
11ms
Poloxamer-linked prodrug of a topoisomerase I inhibitor SN22 shows efficacy in models of high-risk neuroblastoma with primary and acquired chemoresistance. (PubMed, FASEB J)
Together with extended tumor exposure to therapeutically effective drug levels via reversible conjugation to Pluronic F-108 (PF108), these features translated into rapid tumor regression and long-term survival in models of both ABCG2-overexpressing and p53-mutant high-risk neuroblastomas, in contrast to a marginal effect of the clinically used camptothecin derivative, irinotecan. Our results demonstrate that pharmacophore enhancement, increased tumor uptake, and optimally stable carrier-drug association integrated into the design of the hydrolytically activatable PF108-[SN22]  have the potential to effectively combat multiple mechanisms governing chemoresistance in newly diagnosed (chemo-naïve) and recurrent forms of aggressive malignancies. As a macromolecular carrier-based delivery system exhibiting remarkable efficacy against two particularly challenging forms of high-risk neuroblastoma, PF108-[SN22] can pave the way to a robust and clinically viable therapeutic strategy urgently needed for patients with multidrug-resistant disease presently lacking effective treatment options.
Journal
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TP53 (Tumor protein P53) • ABCG2
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TP53 mutation • ABCG2 overexpression
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irinotecan
1year
Journal
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ABCG2
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ABCG2 overexpression
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doxorubicin hydrochloride • mitoxantrone • KU-55933
1year
Tepotinib Inhibits Several Drug Efflux Transporters and Biotransformation Enzymes: The Role in Drug-Drug Interactions and Targeting Cytostatic Resistance In Vitro and Ex Vivo. (PubMed, Int J Mol Sci)
In subsequent drug combination experiments, tepotinib synergistically reversed daunorubicin and mitoxantrone resistance in cells with ABCB1 and ABCG2 overexpression, respectively. Finally, tested drug was observed to have negligible effect on the expression of clinically relevant drug efflux transporters and CYP enzymes. In conclusion, our findings provide complex overview on the tepotinib's drug interaction profile and suggest a promising novel therapeutic strategy for future clinical investigations.
Preclinical • Journal
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ABCB1 (ATP Binding Cassette Subfamily B Member 1) • ABCG2
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ABCG2 overexpression • ABCB1 overexpression
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daunorubicin • Tepmetko (tepotinib) • mitoxantrone
over1year
The Second-Generation PIM Kinase Inhibitor TP-3654 Resensitizes ABCG2-Overexpressing Multidrug-Resistant Cancer Cells to Cytotoxic Anticancer Drugs. (PubMed, Int J Mol Sci)
In this study, we discovered that by attenuating the drug transport function of ABCG2, TP-3654 resensitizes ABCG2-overexpressing multidrug-resistant cancer cells to cytotoxic ABCG2 substrate drugs topotecan, SN-38 and mitoxantrone. Moreover, our results indicate that ABCG2 does not mediate resistance to TP-3654 and may not play a major role in the induction of resistance to TP-3654 in cancer patients. Taken together, our findings reveal that TP-3654 is a selective, potent modulator of ABCG2 drug efflux function that may offer an additional combination therapy option for the treatment of multidrug-resistant cancers.
Journal
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ABCG2
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ABCG2 overexpression
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topotecan • mitoxantrone • TP-3654
over1year
The Spleen Tyrosine Kinase Inhibitor, Entospletinib (GS-9973) Restores Chemosensitivity in Lung Cancer Cells by Modulating ABCG2-mediated Multidrug Resistance. (PubMed, Int J Biol Sci)
In vitro, 3 μM of GS-9973 reversed the drug resistance of NCI-H460/MX20 cell line to mitoxantrone or doxorubicin. Finally, HPLC analysis proved that the intracellular concentration of GS-9973 is not significantly different in both parental and resistant cell lines. In conclusion, our study suggests that in vitro, GS-9973 in combination with certain anticancer drugs, represent a strategy to overcome ABCG2-mediated MDR cancers.
Journal
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ABCG2 • SYK (Spleen tyrosine kinase)
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ABCG2 overexpression
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doxorubicin hydrochloride • entospletinib (GS-9973) • mitoxantrone
over1year
The Cisplatin, 5-fluorouracil, Irinotecan, and Gemcitabine Treatment in Resistant 2D and 3D Model Triple Negative Breast Cancer Cell Line: ABCG2 Expression Data. (PubMed, Anticancer Agents Med Chem)
More resistance to chemotherapeutics and altered gene expression profile was shown in 3D cell cultures when compared with the 2D cells. These results might play an important role to evaluate the efficacy of anticancer drugs, explore mechanisms of MDR in the 3D spheroid forms.
Preclinical • Journal
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ABCG2
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ABCG2 overexpression
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cisplatin • gemcitabine • 5-fluorouracil • irinotecan
over1year
The Novel Benzamide Derivative, VKNG-2, Restores the Efficacy of Chemotherapeutic Drugs in Colon Cancer Cell Lines by Inhibiting the ABCG2 Transporter. (PubMed, Int J Mol Sci)
Finally, VKNG-2 produced a significant concentration-dependent increase in ATPase activity (EC = 2.3 µM). In conclusion, our study suggests that in vitro, VKNG-2 reverses the resistance of S1-M1-80, a cancer cell line resistant to mitoxantrone and SN-38, by inhibiting the efflux function of the ABCG2 transporter.
Preclinical • Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1) • ABCB1 (ATP Binding Cassette Subfamily B Member 1) • ABCG2 • ABCC1 (ATP Binding Cassette Subfamily C Member 1)
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ABCG2 overexpression
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mitoxantrone
almost2years
SMAR1 attenuates the stemness of osteosarcoma cells via through suppressing ABCG2 transcriptional activity. (PubMed, Environ Toxicol)
Moreover, this SMAR1/ABCG2 axis positively regulates the chemotherapeutic sensitivity of OS cells. This work indicates that SMAR1 is a critical suppressor for OS progression through transcriptionally regulating ABCG2 expression.
Journal
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ABCG2 • HDAC2 (Histone deacetylase 2)
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ABCG2 overexpression
almost2years
[VIRTUAL] Shortening of mRNA 3' untranslated region mediates simultaneous overexpression of ABCG2 and CD133 in putative cancer stem cells (AACR 2021)
A novel mRNA 3’UTR shortening machinery was shown to mediate the simultaneous overexpression of ABCG2 and CD133 in SP and CSC cells. It may represent useful drug target for circumvention of resistance and eradication of CSCs.
Late-breaking abstract
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ABCG2 • CD133 • BMI1 (BMI1 proto-oncogene, polycomb ring finger)
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ABCG2 overexpression • CD133 expression • CD133 overexpression