ArticleInternational journal of molecular sciences2018
FK506 Attenuates the MRP1-Mediated Chemoresistant Phenotype in Glioblastoma Stem-Like Cells.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Inhibition of LDHA promotes GSDME-dependent pyroptosis by activating RIG-I-like receptor signaling.Apoptosis : an international journal on programmed cell death · 2026Article
- Reversal gene expression assessment for drug repurposing, a case study of glioblastoma.Journal of translational medicine · 2025Article
- Reversal Gene Expression Assessment for Drug Repurposing, a Case Study of Glioblastoma.Research square · 2024Article
- Review
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- Cancer stem cells and strategies for targeted drug delivery.Drug delivery and translational research · 2021Review
- Review
- Identification of a Metabolism-Related Risk Signature Associated With Clinical Prognosis in Glioblastoma Using Integrated Bioinformatic Analysis.Frontiers in oncology · 2020Article
- Adenosine Depletion as A New Strategy to Decrease Glioblastoma Stem-Like Cells Aggressiveness.Cells · 2019Article
- New Strategies to Overcome Resistance to Chemotherapy and Immune System in Cancer.International journal of molecular sciences · 2019Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Poor response to current treatments for glioblastoma has been attributed to the presence of glioblastoma stem-like cells (GSCs). GSCs are able to expel antitumor drugs to the extracellular medium using the multidrug resistance-associated protein 1 (MRP1) transporter. Tacrolimus (FK506) has been identified as an MRP1 regulator in differentiated glioblastoma (GBM) cells (non-GSCs); however, the effect of FK506 on GSCs is currently unknown. The objective of the following research is to evaluate the effect of FK506 on the MRP1-related chemo-resistant phenotype of GSCs. For this, U87MG and C6 glioma cell lines were used to generate non-GSCs and GSCs. mRNA and MRP1-positive cells were evaluated by RT-qPCR and flow cytometry, respectively. A Carboxyfluorescein Diacetate (CFDA)-retention assay was performed to evaluate the MRP1 activity. Apoptosis and MTT assays were employed to evaluate the cytotoxic effects of FK506 plus Vincristine (MRP1 substrate). GSC-derived subcutaneous tumors were generated to evaluate the in vivo effect of FK506/Vincristine treatment. No differences in transcript levels and positive cells for MRP1 were observed in FK506-treated cells. Lesser cell viability, increased apoptosis, and CFDA-retention in the FK506/Vincristine-treated cells were observed. In vivo, the FK506/Vincristine treatment decreased the tumor size as well as ki67, Glial Fibrillary Acidic Protein (GFAP), and nestin expression. We conclude that FK506 confers a chemo-sensitive phenotype to MRP1-drug substrate in GSCs.
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