Evidence map›Paper›PMID 40772306›Full record

ArticleHistology and histopathology2026

Suppressing SMURF1 to preserve GSTM2: An approach to reducing gastric cancer aggressiveness

Guoming Ma, Jingwu Li, Yuanting Lu, Weiwei Zuo

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Article in Histology and histopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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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

4 authors.

Guoming MaThe First Department of Gastrointestinal Surgery, Tangshan People's Hospital, Tangshan City, Hebei Province, China.
Jingwu LiDepartment of Gastrointestinal Surgery, Tangshan People's Hospital, Tangshan City, Hebei Province, China.
Yuanting LuThe First Department of Gastrointestinal Surgery, Tangshan People's Hospital, Tangshan City, Hebei Province, China.
Weiwei ZuoThe Second Department of Obstetrics and Gynecology, Tangshan People's Hospital, Tangshan City, Hebei Province, China. zuoweiwei_zww@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmad Ubiquitination Regulatory Factor-1 (SMURF1) is implicated in promoting gastric cancer progression by enhancing cell proliferation, migration, and invasion. This study aims to elucidate how SMURF1 drives gastric cancer aggressiveness, with a focus on its interaction with Glutathione S-transferase mu 2 (GSTM2).

methodsBioinformatics analysis identified dysregulated SMURF1 and GSTM2 expression in stomach adenocarcinoma (STAD). The relation between GSTM2 and SMURF1 was predicted using Unibrowser. Functional assays, including cell counting kit-8, wound healing, and Transwell invasion, were conducted on gastric cancer cells to explore the effects of GSTM2 and/or SMURF1. The ubiquitination level of GSTM2 was measured using western blot and immunoprecipitation.

resultsSMURF1 was highly expressed and the GSTM2 level was significantly downregulated in STAD. GSTM2 silencing activated the viability, migration, and invasion of gastric cancer cells, and these cell functions were inhibited by GSTM2 overexpression, which was reversed by SMURF1 overexpression. SMURF1 was predicted to be an E3 ubiquitin ligase for GSTM2. SMURF1 overexpression or Cyclohexanecarboxamide (CHX) addition suppressed GSTM2 levels in gastric cancer cells. Silencing of SMURF1 restrained GSTM2 ubiquitination.

conclusionThis study reveals a novel oncogenic axis, where SMURF1 promotes gastric cancer progression by targeting GSTM2 for degradation. Inhibiting SMURF1 stabilizes GSTM2, leading to reduced cell proliferation, migration, and invasion both

Indexed as

AdenocarcinomaGlutathione TransferaseStomach NeoplasmsUbiquitin-Protein LigasesAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CMice, Nudeglutathione S-transferase Mu 2Glutathione TransferaseSMURF1 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID40772306

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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.