Evidence map›Paper›PMID 40783674›Full record

ArticleDiscover oncology2025

SPINT1-AS1 promotes oxidative damage and apoptosis of gastric cancer cells via the miR-656-3p/PLCXD3 axis.

Duo Xu, Tong Wu, Xin Zhao, ShaoHai Li, XiaoHui Wei

Abstract read
In one paragraph

Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Duo Xu *Weinan Vocational and Technical College, Weinan City, 714026, Shaanxi Province, China.
Tong Wu *Department of Gastroenterology, The Second People's Hospital of Jiulongpo District, Chongqing City, 400050, China.
Xin ZhaoWeinan Vocational and Technical College, Weinan City, 714026, Shaanxi Province, China.
ShaoHai LiWeinan Vocational and Technical College, Weinan City, 714026, Shaanxi Province, China.
XiaoHui WeiDepartment of Medical Oncology, Shaanxi Provincial Cancer Hospital, No.309 Yanta West Road, Yanta District, Xi'an City, 710065, Shaanxi Province, China. weixiao120987@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesIn the study of gastric cancer (GC), long non-coding RNAs (lncRNAs) have been identified and their functions have been partly characterized; however, the specific function of SPINT1 antisense RNA 1 (SPINT1-AS1) in GC remains unclear. This study aimed to investigate the role of SPINT1-AS1 in GC cells and elucidate its downstream molecular mechanisms.

methodsSPINT1-AS1, microRNA-656-3p (miR-656-3p), and phospholipase C, X domain containing 3 (PLCXD3) levels were modulated in GC cells through transfection experiments. Quantitative reverse transcription polymerase chain reaction and Western blot analyses were performed to assess SPINT1-AS1, miR-656-3p, and PLCXD3 levels. The proliferative capacity, apoptosis, invasion, migration, and oxidative stress levels of GC cells were evaluated using 5-ethynyl-2'-deoxyuridine assay, colony formation assay, flow cytometry, Transwell assays, and commercial kits, respectively. Dual-luciferase reporter assay and RNA immunoprecipitation assay were conducted to assess the targeting relationships among SPINT1-AS1, miR-656-3p, and PLCXD3. The impact of SPINT1-AS1 on GC tumor growth was examined in xenograft tumor models.

resultsSPINT1-AS1 and PLCXD3 were found to be downregulated in GC, whereas miR-656-3p was upregulated. SPINT1-AS1 elevation inhibited GC cell proliferation, invasion, migration, and oxidative stress, and promoted apoptosis. SPINT1-AS1 knockdown had opposite effects. The pro-tumor effects induced by SPINT1-AS1 knockdown were reversed by concomitant knockdown of miR-656-3p. Similarly, the inhibitory effects of SPINT1-AS1 elevation on GC malignancy were abrogated by PLCXD3 knockdown. SPINT1-AS1 knockdown suppressed GC tumor growth in mice. SPINT1-AS1 competitively bound to miR-656-3p to mediate PLCXD3 expression.

conclusionsSPINT1-AS1 suppresses GC malignancy through the regulation of the miR-656-3p/PLCXD3 axis. These findings provide robust data supporting the biological functions of lncRNAs in GC and offer potential targets for therapeutic intervention.

Indexed as

Gastric cancermiR-656-3pOxidative damagePLCXD3SPINT1-AS1

Identifiers

PMID40783674
PMCPMC12335420

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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.