Evidence map›Paper›PMID 31096997›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

The regulatory ZFAS1/miR-150/ST6GAL1 crosstalk modulates sialylation of EGFR via PI3K/Akt pathway in T-cell acute lymphoblastic leukemia.

Qianqian Liu, Hongye Ma, Xiuhua Sun, Bing Liu, Yang Xiao, Shimeng Pan, Huimin Zhou, Weijie Dong, Li Jia

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. 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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 64 citations in OpenAlex.

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  4. REMR: Identification of RNA Editing-mediated MiRNA Regulation in Cancers.Computational and structural biotechnology journal · 2024
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  20. Epigenetic Regulation of Glycosylation in Cancer and Other Diseases.International journal of molecular sciences · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Qianqian LiuCollege of Laboratory Medicine, Dalian Medical University, Dalian 116044, 9 Lushunnan Road Xiduan, Dalian, 116044, Liaoning Province, China.
Hongye MaDepartment of Clinical Laboratory, Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital University of Medicine Sciences, Beijing, 100010, China.
Xiuhua SunDepartment of Medicine Oncology, Second Affiliated Hospital of Dalian Medical University, Dalian, 116027, Liaoning Province, China.
Bing LiuCollege of Laboratory Medicine, Dalian Medical University, Dalian 116044, 9 Lushunnan Road Xiduan, Dalian, 116044, Liaoning Province, China.
Yang XiaoCollege of Laboratory Medicine, Dalian Medical University, Dalian 116044, 9 Lushunnan Road Xiduan, Dalian, 116044, Liaoning Province, China.
Shimeng PanCollege of Laboratory Medicine, Dalian Medical University, Dalian 116044, 9 Lushunnan Road Xiduan, Dalian, 116044, Liaoning Province, China.
Huimin ZhouDepartment of Microbiology, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
Weijie DongDepartment of Biochemistry, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
Li JiaCollege of Laboratory Medicine, Dalian Medical University, Dalian 116044, 9 Lushunnan Road Xiduan, Dalian, 116044, Liaoning Province, China. linjian0198@sina.com.
Dalian Medical University · CNBeijing Hospital of Traditional Chinese Medicine · CN

Funding

National Natural Science Foundation of China 81472014
6 · The paper itself

Abstract

backgroundNoncoding RNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are becoming key parts in the development of multidrug resistance (MDR) in T-cell acute lymphoblastic leukemia (T-ALL). Abnormal expression in sialyated N-glycans have been observed in MDR leukemia. However, the role of sialylation regulated MDR remains poorly understood. The aim of this work is to analyze the alternation of N-glycans in T-ALL MDR.

methodsHere, mass spectrometry (MS) is analyzed to screen the N-glycan profiles from ALL cell line CR and adriamycin (ADR)-resistant CR (CR/A) cells. The expression of sialyltransferase (ST) genes in T-ALL cell lines and bone marrow mononuclear cells (BMMCs) of T-ALL patients were analyzed using qRT-PCR. Functionally, T-ALL cell proliferation and MDR are detected through CCK8 assay, colony formation assay, western blot and flow cytometry. RIP assay and Dual-luciferase reporter gene assay confirm the binding association between ZFAS1 and miR-150. Xenograft nude mice models are used to determine the role of ST6GAL1 in vivo.

resultsElevated expression of α2, 6-sialyltransferase 1 (ST6GAL1) has been detected. The altered level of ST6GAL1 was corresponding to the drug-resistant phenotype of T-ALL cell lines both in vitro and in vivo. ZFAS1/miR-150/ST6GAL1 axis was existed in T-ALL cell lines. MiR-150 was downregulated and inversely correlated to ST6GAL1 expression. ZFAS1 was a direct target of miR-150 and positively modulated ST6GAL1 level by binding miR-150. ZFAS1/miR-150/ST6GAL1 axis functioned to regulate ADR-resistant cell growth and apoptosis. Besides, EGFR was demonstrated to be a substrate of ST6GAL1, and the sialylated EGFR had an impact on the PI3K/Akt pathway.

conclusionResults suggested that ZFAS1/miR-150/ST6GAL1 axis involves in the progression of T-ALL/MDR further mediates sialylated EGFR via PI3K/Akt pathway. This work might have an application against T-ALL MDR.

Indexed as

EGFR/PI3K/Akt pathwaymiR-150ST6GAL1T-ALLZFAS1

Identifiers

PMID31096997
PMCPMC6524305
OpenAlexW2947793144

What OpenQuestion holds

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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.