Evidence map›Paper›PMID 35136029›Full record

ArticleCell death & disease2022

LncRNA BC200/miR-150-5p/MYB positive feedback loop promotes the malignant proliferation of myelodysplastic syndrome.

Zhaoping Liu, Pan Wang, Shunling Yuan, Yanyan Wang, Pengfei Cao, Feng Wen, Hui Li, Lin Zhu, Long Liang, Zi Wang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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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

15 authors at 4 institutions in 1 country.

Zhaoping Liu *Department of Clinical Laboratory, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033, Guangdong, China.
Pan Wang *Molecular Biology Research Center & Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, China.
Shunling Yuan *Department of Clinical Laboratory, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033, Guangdong, China.
Yanyan WangThe First Affiliated Hospital, Department of Clinical Laboratory, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Pengfei CaoDepartment of Hematology, Xiangya Hospital, Central South University, Changsha, 410008, China.
Feng WenThe First Affiliated Hospital, Department of Hematology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Hui LiMolecular Biology Research Center & Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, China.ORCID http://orcid.org/0000-0003-1086-0402
Lin ZhuMolecular Biology Research Center & Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, China.
Long LiangMolecular Biology Research Center & Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, China.
Zi WangMolecular Biology Research Center & Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, China.ORCID http://orcid.org/0000-0003-3892-827X
Bin HuMolecular Biology Research Center & Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, China.
Fuxiang ZhengDepartment of Clinical Laboratory, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033, Guangdong, China.
Jing LiuMolecular Biology Research Center & Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, China. liujing2@sklmg.edu.cn.ORCID http://orcid.org/0000-0001-5588-3865
Xiaojuan XiaoMolecular Biology Research Center & Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, China. xiaojuan_xiao@csu.edu.cn.ORCID http://orcid.org/0000-0002-7058-297X
Ji ZhangDepartment of Clinical Laboratory, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033, Guangdong, China. zhang_ji001@hotmail.com.ORCID http://orcid.org/0000-0002-6610-9805
Central South University · CNShenzhen Pingle Orthopedic Hospital · CNUniversity of South China · CNFirst Affiliated Hospital of University of South China · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81770107, 81920108004National Natural Science Foundation of China (National Science Foundation of China) 81870105National Natural Science Foundation of China (National Science Foundation of China) 81970195National Natural Science Foundation of China (National Science Foundation of China) 82003286
6 · The paper itself

Abstract

Myelodysplastic syndrome (MDS) is a group of heterogeneous hematologic malignancies with a risk of transformation to acute myeloid leukemia. Understanding the molecular mechanisms of the specific roles of long noncoding RNAs (lncRNAs) in MDS would create novel ways to identify diagnostic and therapeutic targets. The lncRNA BC200 is upregulated and acts as an oncogene in various cancers; however, its expression, clinical significance, and roles in MDS remain unclear. Here, we found that BC200 was highly expressed in MDS patients compared with normal individuals. Knockdown of BC200 inhibited MDS cell proliferation, colony formation, and cell cycle progression in vitro and suppressed the growth and invasiveness of MDS cells in vivo. Mechanistic investigations revealed that BC200 functioned as a miRNA sponge to positively regulate the expression of MYB through sponging miR-150-5p and subsequently promoted malignant proliferation of MDS cells. Conversely, we found that BC200 was a direct transcriptional target of MYB, and knockdown of MYB abolished the oncogenic effect of BC200/miR-150-5p. Taken together, our results revealed that the BC200/miR-150-5p/MYB positive feedback loop promoted the proliferation of MDS cells and is expected to be a potential biomarker and therapeutic target in MDS.

Indexed as

MicroRNAsMyelodysplastic SyndromesProto-Oncogene Proteins c-mybRNA, Long NoncodingCell Line, TumorCell MovementCell ProliferationFeedbackGene Expression Regulation, NeoplasticHumansMicroRNAsMIR150, humanMYB protein, humanProto-Oncogene Proteins c-mybRNA, Long Noncoding

Identifiers

PMID35136029
PMCPMC8825806
OpenAlexW4210835862

What OpenQuestion holds

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LicenceCC BY
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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.