ArticleCancer science2020
Dual TTK/CLK2 inhibitor, CC-671, selectively antagonizes ABCG2-mediated multidrug resistance in lung cancer cells.
Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Review
- Mitotic Machinery Dysregulation in Lung Cancer: Biological Roles, Therapeutic Targeting, and Combination Strategies.Pharmaceutics · 2026Review
- B-9-8, a Novel Harman Dimer, Reverses ABCG2-mediated Chemotherapeutic Drug Resistance.Recent patents on anti-cancer drug discovery · 2026Article
- RNA processing kinase inhibitors and epigenetic inhibitors in combination with oncology drugs or investigational agents in multi-cell type patient-derived tumor cell line spheroids.Cancer chemotherapy and pharmacology · 2025Article
- Upregulation of TTK expression is associated with poor prognosis and immune infiltration in endometrial cancer patients.Cancer cell international · 2024Article
- Advances in the structure, mechanism and targeting of chemoresistance-linked ABC transporters.Nature reviews. Cancer · 2023Review
- Enzyme-catalyzed synthesis of selenium-doped manganese phosphate for synergistic therapy of drug-resistant colorectal cancer.Journal of nanobiotechnology · 2023Article
- MET inhibitor tepotinib antagonizes multidrug resistance mediated by ABCG2 transporter:Acta pharmaceutica Sinica. B · 2022Article
- ABCB1 limits the cytotoxic activity of TAK-243, an inhibitor of the ubiquitin-activating enzyme UBA1.Frontiers in bioscience (Landmark edition) · 2022Article
- Association of Angiogenesis Gene Expression With Cancer Prognosis and Immunotherapy Efficacy.Frontiers in cell and developmental biology · 2022Article
- The Resistance of Cancer Cells to Palbociclib, a Cyclin-Dependent Kinase 4/6 Inhibitor, is Mediated by the ABCB1 Transporter.Frontiers in pharmacology · 2022Article
- Comprehensive analysis of the prognostic value and immune implications of the TTK gene in lung adenocarcinoma: a meta-analysis and bioinformatics analysis.Animal cells and systems · 2022Article
- Scaffold fragmentation and substructure hopping reveal potential, robustness, and limits of computer-aided pattern analysis (C@PA).Computational and structural biotechnology journal · 2021Article
- Overexpression of ABCG2 Confers Resistance to MLN7243, a Ubiquitin-Activating Enzyme (UAE) Inhibitor.Frontiers in cell and developmental biology · 2021Article
- Article
- BMS-599626, a Highly Selective Pan-HER Kinase Inhibitor, Antagonizes ABCG2-Mediated Drug Resistance.Cancers · 2020Article
- Dual TTK/CLK2 inhibitor, CC-671, selectively antagonizes ABCG2-mediated multidrug resistance in lung cancer cells.Cancer science · 2020Article
- Reversal of Cancer Multidrug Resistance (MDR) Mediated by ATP-Binding Cassette Transporter G2 (ABCG2) by AZ-628, a RAF Kinase Inhibitor.Frontiers in cell and developmental biology · 2020Article
- Establishment and Characterization of an Irinotecan-Resistant Human Colon Cancer Cell Line.Frontiers in oncology · 2020Article
- Elevated ABCB1 Expression Confers Acquired Resistance to Aurora Kinase Inhibitor GSK-1070916 in Cancer Cells.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
One pivotal factor that leads to multidrug resistance (MDR) is the overexpression of ABCG2. Therefore, tremendous effort has been devoted to the search of effective reversal agents to overcome ABCG2-mediated MDR. CC-671 is a potent and selective inhibitor of both TTK (human protein kinase monopolar spindle 1 [hMps1]) and CDC like kinase 2 (CLK2). It represents a new class of cancer therapeutic drugs. In this study, we show that CC-671 is an effective ABCG2 reversal agent that enhances the efficacy of chemotherapeutic drugs in ABCG2-overexpressing lung cancer cells. Mechanistic studies show that the reversal effect of CC-671 is primarily attributed to the inhibition of the drug efflux activity of ABCG2, which leads to an increased intracellular level of chemotherapeutic drugs. In addition, CC-671 does not alter the protein expression or subcellular localization of ABCG2. The computational molecule docking analysis suggests CC-671 has high binding affinity to the drug-binding site of ABCG2. In conclusion, we reveal the interaction between CC-671 and ABCG2, providing a rationale for the potential combined use of CC-671 with ABCG2 substrate to overcome MDR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.