ArticleBMC cancer2012
Wnt/β-catenin pathway regulates ABCB1 transcription in chronic myeloid leukemia.
Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 101 citations in OpenAlex.
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- Development and Validation of a Sensitive and Specific LC-MS/MS Method for IWR-1-Endo, a Wnt Signaling Inhibitor: Application to a Cerebral Microdialysis Study.Molecules (Basel, Switzerland) · 2022Article
- A model for the intrinsic limit of cancer therapy: Duality of treatment-induced cell death and treatment-induced stemness.PLoS computational biology · 2022Article
- Chemotherapy induces feedback up-regulation of CD44v6 in colorectal cancer initiating cells throughFrontiers in oncology · 2022Article
- Fzd7/Wnt7b signaling contributes to stemness and chemoresistance in pancreatic cancer.Cancer medicine · 2021Article
- Advanced bioinformatic analysis and pathway prediction of NSCLC cells upon cisplatin resistance.Scientific reports · 2021Article
- Cancer stem cells in colorectal cancer and the association with chemotherapy resistance.Medical oncology (Northwood, London, England) · 2021Review
- Shc3 promotes hepatocellular carcinoma stemness and drug resistance by interacting with β-catenin to inhibit its ubiquitin degradation pathway.Cell death & disease · 2021Article
- ABCB1 and ABCG2 restricts the efficacy of gedatolisib (PF-05212384), a PI3K inhibitor in colorectal cancer cells.Cancer cell international · 2021Article
- Conditional genetic deletion of CSF1 receptor in microglia ameliorates the physiopathology of Alzheimer's disease.Alzheimer's research & therapy · 2021Article
- Teaching an old dog new tricks: reactivated developmental signaling pathways regulate ABCB1 and chemoresistance in cancer.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- A20 and RBX1 Regulate Brentuximab Vedotin Sensitivity in Hodgkin Lymphoma Models.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe advanced phases of chronic myeloid leukemia (CML) are known to be more resistant to therapy. This resistance has been associated with the overexpression of ABCB1, which gives rise to the multidrug resistance (MDR) phenomenon. MDR is characterized by resistance to nonrelated drugs, and P-glycoprotein (encoded by ABCB1) has been implicated as the major cause of its emergence. Wnt signaling has been demonstrated to be important in several aspects of CML. Recently, Wnt signaling was linked to ABCB1 regulation through its canonical pathway, which is mediated by β-catenin, in other types of cancer. In this study, we investigated the involvement of the Wnt/β-catenin pathway in the regulation of ABCB1 transcription in CML, as the basal promoter of ABCB1 has several β-catenin binding sites. β-catenin is the mediator of canonical Wnt signaling, which is important for CML progression.
methodsIn this work we used the K562 cell line and its derived MDR-resistant cell line Lucena (K562/VCR) as CML study models. Real time PCR (RT-qPCR), electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation (ChIP), flow cytometry (FACS), western blot, immunofluorescence, RNA knockdown (siRNA) and Luciferase reporter approaches were used.
resultsβ-catenin was present in the protein complex on the basal promoter of ABCB1 in both cell lines in vitro, but its binding was more pronounced in the resistant cell line in vivo. Lucena cells also exhibited higher β-catenin levels compared to its parental cell line. Wnt1 and β-catenin depletion and overexpression of nuclear β-catenin, together with TCF binding sites activation demonstrated that ABCB1 is positively regulated by the canonical pathway of Wnt signaling.
conclusionsThese results suggest, for the first time, that the Wnt/β-catenin pathway regulates ABCB1 in CML.
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