Evidence map›Paper›PMID 40837760›Full record

ArticleWorld journal of gastrointestinal oncology2025

LncRNA SNHG5 modulates cell proliferation and migration through the miR-92a-3p/BTG2 axis in gastric cancer by the PI3K/AKT pathway.

Qi-Qi Mao, Mei-Lin Zhang, Liang Zhong, Xu-Dong Xu, Xin-Hai Wang, Du-Yi Pan, Fu-Sheng Zhou, Jia-Xin Huang, Xian-Guang Zhao, Jia-Jie Chen and 3 more

Abstract read
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In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Research progress on BTG2 in non‑tumor diseases (Review).International journal of molecular medicine · 2026
    Review
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

13 authors.

Qi-Qi MaoDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Mei-Lin ZhangDepartment of Pathology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Liang ZhongDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China. ifb422@yeah.net.
Xu-Dong XuDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Xin-Hai WangDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai 201907, China.
Du-Yi PanDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Fu-Sheng ZhouDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Jia-Xin HuangDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Xian-Guang ZhaoDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Jia-Jie ChenDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Xiao-Yun JiangDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Xu SunDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Wei-Qun DingDepartment of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGastric cancer (GC) is a widespread malignancy and associated with high rates of morbidity and mortality worldwide.

aimTo examine the functional role of long non-coding RNAs small nucleolar RNA host gene 5 (SNHG5) and its regulation of miR-92a-3p and B-cell translocation gene 2 (BTG2) in GC progression.

methodsQuantitative reverse transcription PCR and western blot analysis determined the expression of SNHG5, miR-92a-3p, and BTG2 in GC and adjacent non-neoplastic mucosa. Dual-luciferase assays demonstrated interactions of SNHG5 with miR-92a-3p and BTG2. AGS cells were transfected with SNHG5 overexpression and miR-92a-3p knockdown models. Various assays, including CCK-8, colony formation, scratch wound healing, and Transwell assays, were used to determine cell proliferation and migration. An experimental model of a xenograft mouse was used to determine

resultsBTG2 and SNHG5 were downregulated in GC tissues, and miR-92a-3p was upregulated. Overexpression of SNHG5 or knockdown of miR-92a-3p reduced GC cell proliferation and migration, and increased BTG2 expression while decreasing PI3K/AKT signaling activity. The dual-luciferase assays demonstrated direct binding of miR-92a-3p to SNHG5 and BTG2. Tumor volume and weight were significantly reduced in mice transplanted with AGS cells treated with miR-92a-3p inhibitor or SNHG5 overexpression compared with control AGS cells. Hematoxylin and eosin staining revealed that treated tumors exhibited degenerative characteristics, including irregular morphology and nucleolysis.

conclusionLncRNA SNHG5 inhibited GC cell growth and migration by modulating the PI3K/AKT pathway

Indexed as

B-cell translocation gene 2Cell proliferationGastric cancerLong non-coding RNAs small nucleolar RNA host gene 5Non-coded RNAPI3K/AKT signaling pathway

Identifiers

PMID40837760
PMCPMC12362537

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