Evidence map›Paper›PMID 40248062›Full record

ArticleWorld journal of gastroenterology2025

Long noncoding RNA semaphorin 6A-antisense RNA 1 reduces hepatocellular carcinoma by promoting semaphorin 6A mRNA degradation.

Song-Man Yu, Min Zhang, Sha-Lin Li, Si-Ya Pei, Li Wu, Xing-Wang Hu, Yan-Kun Duan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. SEMA6A overexpression inhibited tumor growth and metastasis in colorectal cancer.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    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

7 authors.

Song-Man YuDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China.
Min ZhangDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China.
Sha-Lin LiDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China.
Si-Ya PeiDepartment of Blood Transfusion, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China.
Li WuDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China.
Xing-Wang HuDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China.
Yan-Kun DuanDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China. ykduan@csu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is a prevalent malignant tumor with a poor prognosis, which is often associated with chronic hepatitis B virus infection in China. Our previous study has shown that long non-coding RNA semaphorin 6A-antisense RNA 1 (SEMA6A-AS1) was significantly downregulated in hepatitis B virus-related HCC and associated with poor prognosis.

aimTo explore the underlying mechanism of SEMA6A-AS1 in HCC progression.

methodsThe expression levels of SEMA6A-AS1 and SEMA6A were detected using quantitative polymerase chain reaction, immunohistochemistry and Western blot. A growth curve, colony formation, wound-healing and transwell (with or without Matrigel) assays were respectively performed to assess the proliferation, migration and invasion abilities of HCC cells. Cell cycle and apoptosis assays were performed by flow cytometry. To investigate the potential mechanism underpinning SEMA6A-AS1, we utilized tagged RNA affinity purification, dual luciferase reporter assay and immunofluorescence.

resultsDownregulation of SEMA6A-AS1 in HCC was negatively correlated with SEMA6A protein expression. SEMA6A was upregulated in HCC and correlated with high alpha-fetoprotein level, high Edmondson-Steiner grade and poor prognosis. SEMA6A-AS1 significantly inhibited the proliferation, migration and invasion of HCC cells by combining with SEMA6A mRNA and promoting its degradation. SEMA6A protein promoted the proliferation, migration and invasion of HCC cells by regulating the actin cytoskeleton.

conclusionOur findings suggest that SEMA6A-AS1 can inhibit HCC progression through decreasing SEMA6A expression by promoting its mRNA degradation. SEMA6A-AS1 may be a prognostic biomarker and therapeutic target for HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsRNA, Long NoncodingSemaphorinsApoptosisCell Line, TumorCell MovementCell ProliferationDisease ProgressionDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedNeoplasm InvasivenessRNA, Long NoncodingRNA, MessengerSemaphorinsHepatocellular carcinomaLiver cancerLong noncoding RNASemaphorin 6ASemaphorin 6A antisense RNA 1

Identifiers

PMID40248062
PMCPMC12001175

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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.