Evidence map›Paper›PMID 35178087›Full record

ArticleJournal of oncology2022

LncRNA UCA1 Promotes the Progression of AML by Upregulating the Expression of CXCR4 and CYP1B1 by Affecting the Stability of METTL14.

Jiajia Li, Zhongyu Li, Xue Bai, Xiaofeng Chen, Meng Wang, Yanping Wu, Haotian Wu

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Journal of oncology, 2022. 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  9. Chidamide inhibits cell glycolysis in acute myeloid leukemia by decreasing N6-methyladenosine-related GNAS-AS1.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2024
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  11. Small molecule inhibitors targeting mJournal of hematology & oncology · 2024
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  13. Non-coding RNA-Mediated N6-Methyladenosine (mNon-coding RNA research · 2024
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  15. Novel insights into mutual regulation between NCancer cell international · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Jiajia LiDepartment of Hematology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, China.ORCID https://orcid.org/0000-0003-4694-0789
Zhongyu LiDepartment of Hematology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, China.
Xue BaiDepartment of Hematology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, China.
Xiaofeng ChenDepartment of Hematology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, China.
Meng WangDepartment of Hematology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, China.
Yanping WuDepartment of Hematology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, China.
Haotian WuBengbu Medical College, Bengbu, Anhui 233030, China.
First Affiliated Hospital of Bengbu Medical College · CNBengbu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIncreasing numbers of studies have proved that m6A methylation plays crucial roles in different cancers. However, how lncRNA regulates m6A methylation and participates in acute myeloid leukemia (AML) remains unclear. Therefore, this study aims to explore the function and mechanism of UCA1 in AML by regulating m6A methylation.

methodsqRT-PCR, western blot, and immunohistochemical staining were used to detect the expression of METTL14, CXCR4, and CYP1B1. qRT-PCR was used to detect the expression of UCA1. CCK8, flow cytometry, and transwell assays were used to detect the proliferation, apoptosis, migration, and invasion of HL60 and U937 cells, respectively. m6A methylation was detected by dot blot analysis. Tumor-bearing mice were established, and tumor weight and volume were analyzed. Immunofluorescence staining, co-localization, and RNA pull-down were used to confirm the reaction between UCA1 and METTL14.

resultsOverexpression of UCA1 promotes AML development

conclusionIn the present study, we demonstrated that lncRNAUCA1 promotes the progression of AML by upregulating the expression of CXCR4 and CYP1B1 by affecting the stability of METTL14.

Identifiers

PMID35178087
PMCPMC8847036
OpenAlexW4210823851

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Registered trials

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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.