ArticleJournal of biosciences2019
ABCG2 aptamer selectively delivers doxorubicin to drug-resistant breast cancer cells.
Article in Journal of biosciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 21 citations in OpenAlex.
- Advances in the structure, mechanism and targeting of chemoresistance-linked ABC transporters.Nature reviews. Cancer · 2023Review
- Quinacrine and Curcumin in combination decreased the breast cancer angiogenesis by modulating ABCG2 via VEGF A.Journal of cell communication and signaling · 2023Article
- Pharmacogenetics of Drug Metabolism: The Role of Gene Polymorphism in the Regulation of Doxorubicin Safety and Efficacy.Cancers · 2022Review
- Aptamer‑based therapy for targeting key mediators of cancer metastasis (Review).International journal of oncology · 2022Review
- Cancer stem cells and strategies for targeted drug delivery.Drug delivery and translational research · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemotherapy is the most widely used treatment for cancer therapy, but its efficacy is limited by the side effects of non-specific cytotoxic drugs. Ligand-based targeting drug-delivery system is a solution to circumvent this issue. In this study, an ABCG2 aptamer-doxorubicin complex was prepared, and its efficacy in targeted drug delivery tomitoxantrone-resistance breast cancer cell line (MCF7/MX) was evaluated. The formation of aptamer-doxorubicin physical complex was analyzed by fluorometric analysis. The cytotoxicities of doxorubicin and aptamer-doxorubicin complex on MCF7 and MCF7/MX cell lines were evaluated by the MTT assay, and IC50 values were obtained. Cellular uptake of aptamer-doxorubicin complex was assessed by flow cytometry cellular uptake assay. Results: Fluorometric analysis of aptamer-doxorubicin showed 1-1.5 molar ratio of the drug to the aptamer could efficiently quenchDox fluorescence.MTTassay results showed that MCF7/MXcells were more resistant to doxorubicin than MCF7 cells (IC50 : 3.172 +/- 0.536 and 1.456 +/- 0.154 μM, respectively). Flow cytometry andMTTassay results showed that the aptamer-doxorubicin complex could increase the uptake and cytotoxicity of doxorubicin inMCF7/MX cell line in comparisonwith free doxorubicin, while the same treatments had no effect on IC50 of Dox on MCF7 cells. The results proposed that the ABCG2 aptamer-drug complex can be effectively used for specific drug delivery to ABCG2-overexpressing cells.
Indexed as
Identifiers
31180052W2938343312What OpenQuestion holds
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.