Evidence mapPaperPMID 34983308Full record

ArticleBioengineered2022

ETS Proto-Oncogene 1-activated muskelin 1 antisense RNA drives the malignant progression of hepatocellular carcinoma by targeting miR-22-3p to upregulate ETS Proto-Oncogene 1.

Guozheng Pan, Jian Zhang, Faping You, Tao Cui, Peng Luo, Shuling Wang, Xiaomei Li, Qingzhong Yuan

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
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  11. Making Sense of Antisense lncRNAs in Hepatocellular Carcinoma.International journal of molecular sciences · 2023
    Review
  12. Article
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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

8 authors at 3 institutions in 2 countries.

Guozheng PanDepartment of Hepatobiliary Sugery, Shengli Oilfield Central Hospital, Dongying, China.
Jian ZhangDepartment of Hepatobiliary Sugery, Shengli Oilfield Central Hospital, Dongying, China.
Faping YouDepartment of Hepatobiliary Sugery, Shengli Oilfield Central Hospital, Dongying, China.
Tao CuiDepartment of Hepatobiliary Sugery, Shengli Oilfield Central Hospital, Dongying, China.
Peng LuoDepartment of Sales, Shanghai Topgen Biopharm Company Ltd, shanghai, china.
Shuling WangDepartment of Hepatobiliary Sugery, Shengli Oilfield Central Hospital, Dongying, China.
Xiaomei LiDepartment of Medical Record, People Hospital of Dongying, Dongying, China.
Qingzhong YuanDepartment of Hepatobiliary Sugery, Shengli Oilfield Central Hospital, Dongying, China.
Shengli Oilfield Central Hospital · CNBiopharma Technology (United Kingdom) · GBDongyang People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNA muskelin 1 antisense RNA (MKLN1-AS) acted as an oncogenic regulator in hepatocellular carcinoma (HCC). This study was performed to investigate the functional mechanism of MKLN1-AS. MKLN1-AS, microRNA-22-3p (miR-22-3p) and ETS Proto-Oncogene 1 (ETS1) levels were examined using reverse transcription-quantitative polymerase-chain reaction. Protein expression was detected by Western blot. The target relation was analyzed by dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. Cell proliferation ability was determined through cell counting kit-8 assay, colony formation assay and ethylenediurea assay. Angiogenesis was examined by tube formation assay. Cell migration and invasion were assessed via transwell assay. In vivo research was conducted by xenograft tumor model in nude mice. MKLN1-AS was upregulated in HCC tissues and cells. ETS1 promoted the ETS1 expression by binding to the 582-596 sites. Silence of MKLN1-AS suppressed cell growth, angiogenesis, migration, and invasion. MKLN1-AS interacted with miR-22-3p in HCC cells. The function of MKLN1-AS downregulation was relieved by miR-22-3p inhibition in HCC cells. ETS1 was validated as a target of miR-22-3p, and MKLN1-AS upregulated the ETS1 expression by sponging miR-22-3p. Overexpression of miR-22-3p retarded HCC progression by downregulating the level of ETS1. Tumor growth in vivo was also enhanced by MKLN1-AS through the regulation of miR-22-3p/ETS1 axis. These data demonstrated that ETS1-mediated MKLN1-AS contributed to the malignant phenotypes of HCC cells via depending on the miR-22-3p/ETS1 regulatory axis.

Indexed as

AnimalsCarcinoma, HepatocellularCase-Control StudiesCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMiceMicroRNAsNeoplasm TransplantationProto-Oncogene Protein c-ets-1ETS1 protein, humanMicroRNAsMIRN22 microRNA, humanProto-Oncogene Protein c-ets-1RNA, Long NoncodingETS1hepatocellular carcinomamiR-22-3pMKLN1-AS

Identifiers

PMID34983308
PMCPMC8805956
OpenAlexW4206521717

What Socratic holds

Textmetadata
LicenceCC BY-NC
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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 Socratic graph.