ArticlePloS one2017
GATA2 Inhibition Sensitizes Acute Myeloid Leukemia Cells to Chemotherapy.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 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.
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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
10 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Screening of drug targets for tuberculosis on the basis of transcription factor regulatory network and mRNA sequencing technology.Frontiers in molecular biosciences · 2024Article
- Glycosphingolipid-Glycan Signatures of Acute Myeloid Leukemia Cell Lines Reflect Hematopoietic Differentiation.Journal of proteome research · 2022Article
- A CGA/EGFR/GATA2 positive feedback circuit confers chemoresistance in gastric cancer.The Journal of clinical investigation · 2022Article
- Ventx Family and Its Functional Similarities with Nanog: Involvement in Embryonic Development and Cancer Progression.International journal of molecular sciences · 2022Review
- Inhibition of GATA2 restrains cell proliferation and enhances apoptosis and chemotherapy mediated apoptosis in human GATA2 overexpressing AML cells.Scientific reports · 2019Article
- Targeting an RNA-Binding Protein Network in Acute Myeloid Leukemia.Cancer cell · 2019Article
- Xbra and Smad-1 cooperate to activate the transcription of neural repressor ventx1.1 in Xenopus embryos.Scientific reports · 2018Article
- GATA2 regulates the erythropoietin receptor in t(12;21) ALL.Oncotarget · 2017Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance constitutes one of the main obstacles for clinical recovery of acute myeloid leukemia (AML) patients. Therefore, the treatment of AML requires new strategies, such as adding a third drug. To address whether GATA2 could act as a regulator of chemotherapy resistance in human leukemia cells, we observed KG1a cells and clinical patients' AML cells with a classic drug (Cerubidine) and Gefitinib. After utilizing chemotherapy, the expression of GATA2 and its target genes (EVI, SCL and WT1) in surviving AML cells and KG1a cells were significantly enhanced to double and quadrupled compared to its original level respectively. Furthermore, with continuous chemotherapeutics, AML cells with GATA2 knockdown or treated with GATA2 inhibitor (K1747) almost eliminated with dramatically reduced expression of WT1, SCL, EVI, and significantly increased apoptotic population. Therefore, we propose that reducing GATA2 expression or inhibition of its transcription activity can relieve the drug resistance of acute myeloid leukemia cells and it would be helpful for eliminating the leukemia cells in patients.
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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.