Evidence map›Paper›PMID 38602284›Full record

ArticleImmunity, inflammation and disease2024

LncRNA MIR100HG affects the proliferation and metastasis of lung cancer cells through mediating the microRNA-5590-3p/DCBLD2 axis.

Shengping Min, Linxiang Zhang, Li Zhang, Fangfang Liu, Miao Liu

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 6 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

5 authors at 2 institutions in 1 country.

Shengping MinDepartment of Microbiology and Parasitology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China.
Linxiang ZhangDepartment of Pulmonary and Critical Care Medicine, First Affiliated Hospital, Bengbu Medical College, Anhui Province Key Laboratory of Clinical and Preclinical Research in Respiratory Disease, Bengbu, Anhui, China.
Li ZhangDepartment of Pulmonary and Critical Care Medicine, First Affiliated Hospital, Bengbu Medical College, Anhui Province Key Laboratory of Clinical and Preclinical Research in Respiratory Disease, Bengbu, Anhui, China.
Fangfang LiuDepartment of Pulmonary and Critical Care Medicine, First Affiliated Hospital, Bengbu Medical College, Anhui Province Key Laboratory of Clinical and Preclinical Research in Respiratory Disease, Bengbu, Anhui, China.
Miao LiuDepartment of Microbiology and Parasitology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China.ORCID 0009-0004-4235-9000
First Affiliated Hospital of Bengbu Medical College · CNAnhui Medical University · CN

Funding

Health Research Program of Anhui AHWJ2023A20289Open Resesrch Fund Project of Anhui Province Key Laboratory of Clinical and Preclinical Research in Respiratory Disease HX2023D01Science Research Project of Bengbu Medical College 2022byzd032
6 · The paper itself

Abstract

objectiveThe aim of this paper is to investigate the effect of long noncoding RNA (lncRNA) MIR100HG on the proliferation and metastasis of lung cancer cells by mediating the microRNA (miR)-5590-3p/DCBLD2 axis.

methodsRNA levels of MIR100HG, miR-5590-3p, and DCBLD2 in lung cancer tissues and cells were detected by quantitative reverse-transcription polymerase chain reaction, and protein level was assessed by Western blot. Effects of MIR100HG or miR-5590-3p on proliferation, migration, and invasion of lung cancer cells were detected by Cell Counting Kit-8, colony formation, and Transwell assays. Luciferase reporter assay and RNA-immunoprecipitation assay confirmed the target relationship between miR-5590-3p and MIR100HG or DCBLD2.

resultsMIR100HG and DCBLD2 were highly expressed, while miR-5590-3p was lowly expressed in lung cancer tissues and cells. Silencing MIR100HG or upregulating miR-5590-3p impeded lung cancer cell proliferation, migration, and invasion. MIR100HG could up-regulate DCBLD2 by sponging miR-5590-3p. Downregulation of miR-5590-3p partly overturned the suppressive effect of silencing MIR100HG on lung cancer cell proliferation and metastasis, and overexpression of DCBLD2 also reversed the effect of overexpression of miR-5590-3p on lung cancer cell proliferation and metastasis.

conclusionLncRNA MIR100HG promotes lung cancer progression by targeting and negatively regulating DCBLD2 through binding with miR-5590-3p.

Indexed as

Lung NeoplasmsMicroRNAsRNA, Long NoncodingCell Line, TumorCell MovementCell ProliferationHumansMembrane ProteinsDCBLD2 protein, humanMembrane ProteinsMicroRNAsRNA, Long NoncodingDCBLD2lncRNA MIR100HGlung cancermetastasismiR‐5590‐3pproliferation

Identifiers

PMID38602284
PMCPMC11007817
OpenAlexW4394726251

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.