Evidence map›Paper›PMID 32982274›Full record

ArticleOncoTargets and therapy2020

Long Non-Coding RNA Taurine Upregulated Gene 1 Targets miR-185 to Regulate Cell Proliferation and Glycolysis in Acute Myeloid Leukemia Cells in vitro.

Weide Zhang, Yuhua Liu, Jing Zhang, Ni Zheng

Abstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. 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
    Article
  4. Review
  5. Role of long noncoding RNA taurine-upregulated gene 1 in cancers.Molecular medicine (Cambridge, Mass.) · 2021
    Review
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Weide Zhang *Department of Hematology, The People's Hospital of Shouguang, Shouguang, Shandong, People's Republic of China.
Yuhua Liu *Department of Digestive Oncology, The Gansu Provincial Cancer Hospital, Lanzhou, Gansu, People's Republic of China.
Jing ZhangDepartment of Psychiatry, Shouguang Mental and Health Care Center, Shouguang, Shandong, People's Republic of China.
Ni ZhengDepartment of Clinical Laboratory, Shengli Oilfield Central Hospital, Dongying, Shandong, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute myeloid leukemia (AML) is a group of malignant hematopoietic system diseases. Taurine-upregulated gene 1 (TUG1) is a long non-coding RNA that has been associated with human cancers, including AML. However, the role and molecular mechanisms of TUG1 in AML remains to be defined.

methodsExpression of TUG1 and miR-185 was detected using RT-qPCR. Cell viability and apoptotic rate were measured by MTT assay and flow cytometry, respectively. Glycolysis was determined by commercial glucose and lactate assay kits and Western blot. The target binding between TUG1 and miR-185 was predicted on Starbase online database and confirmed by luciferase reporter assay and RNA immunoprecipitation.

resultsTUG1 was upregulated and miR-185 was downregulated in the peripheral blood mononuclear cells of AML specimens and cells (HL-60, KG-1, MOLM-14, and MOLM-13). Both TUG1 knockdown and miR-185 overexpression via transfection could suppress cell viability, glucose consumption, lactate production, and hexokinase 2 expression, but promote apoptotic rate in HL-60 and KG-1 cells. Notably, TUG1 functioned as a sponge of miR-185 by target binding. Moreover, downregulation of miR-185 could partially overturn the effect of TUG1 knockdown on cell proliferation and glycolysis in HL-60 and KG-1 cells.

conclusionExpression of TUG1 was upregulated in AML patients and cells, and its knockdown repressed cell proliferation and glycolysis in AML cells in vitro by targeting miR-185.

Indexed as

AMLglycolysismiR-185TUG1

Identifiers

PMID32982274
PMCPMC7493018

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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.