ArticleOncology reports2023
NDRG3 regulates imatinib resistance by promoting β‑catenin accumulation in the nucleus in chronic myelogenous leukemia.
Article in Oncology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 4 citations in OpenAlex.
- NDRG3 is essential for sustaining antigen-driven T cell responses by protecting against restimulation-induced cell death.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
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Authors and funding
13 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imatinib resistance in chronic myelogenous leukemia (CML) is a clinical problem. The present study examined the role of N‑Myc downstream regulatory gene 3 (NDRG3) in imatinib resistance in CML. Quantitative PCR demonstrated that NDRG3 was highly expressed in patients with CML. Cell Counting Kit (CCK)‑8 experiments proved that NDRG3 promoted the proliferation of K562 CML cells and enhanced imatinib resistance. Dual‑luciferase assay showed that microRNA (miR)‑204‑5p inhibited expression of NDRG3 and immunofluorescence experiments showed that NDRG3 promoted accumulation of β‑catenin in the nucleus, thereby increasing the expression of downstream drug resistance‑ and cell cycle‑associated factors (c‑Myc and MDR1). At the same time, cell proliferation experiments showed that β‑catenin played a role in cell proliferation and drug resistance. Co‑transfection with small interfering (si)‑β‑catenin partially reversed the effect of NDRG3. This finding indicated that NDRG3 plays an important role in imatinib resistance and miR‑204‑5p and β‑catenin are involved in the biological behavior of NDRG3. The present results provide theoretical support for overcoming drug resistance in CML.
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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.