Evidence map›Paper›PMID 41121403›Full record

ArticleEuropean journal of medical research2025

TIGD6 in gastric cancer: exploring its prognostic value and therapeutic potential through molecular and clinical investigations.

Quanli Han, Muhong Deng, Zhi Cui, Qi Wang, Dongbing Li

Abstract read
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Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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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

5 authors.

Quanli Han *Medical Oncology Department, The First Medical Center, Chinese PLA General Hospital, No.28 Fuxing Road, Haidian District, Beijing, 100953, China. hanquanli@301hospital.com.cn.
Muhong Deng *Medical Oncology Department, The First Medical Center, Chinese PLA General Hospital, No.28 Fuxing Road, Haidian District, Beijing, 100953, China.
Zhi Cui *Medical Oncology Department, The First Medical Center, Chinese PLA General Hospital, No.28 Fuxing Road, Haidian District, Beijing, 100953, China.
Qi Wang *Medical Oncology Department, The First Medical Center, Chinese PLA General Hospital, No.28 Fuxing Road, Haidian District, Beijing, 100953, China.
Dongbing LiScientific Research Center, Beijing ChosenMed Clinical Laboratory Co., Ltd., Beijing, 100176, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGastric cancer (GC) predominantly contributes to cancer mortality, with adenocarcinomas accounting for more than 95% of incidences. Early detection improves survival, but most cases are diagnosed at advanced stages due to subtle symptoms and rapid progression. The role of TIGD6 in GC is unclear.

methodsWe analyzed TIGD6 expression using TCGA data and correlated it with clinical features and outcomes in GC patients. Bioinformatics tools, including GSEA and single-cell sequencing, were used to elucidate TIGD6's role in GC. In the GC cell lines AGS and HGC-27, TIGD6 was knocked down using RNA interference, and subsequent in vitro experiments were conducted to evaluate cell proliferation, migration, and invasion capabilities.

resultsThe expression of TIGD6 was markedly elevated in GC tissues relative to normal tissues (p < 0.001). Higher TIGD6 levels were linked to residual tumors (p = 0.027), history of reflux (p = 0.019), and antireflux treatment (p = 0.0012). Increased TIGD6 expression was associated with decreased overall survival (OS, p = 0.009) and disease-specific survival (DSS, p = 0.008), and it served as an independent predictor of worse OS (p = 0.043). Knocking down TIGD6 in GC cells suppressed proliferation, migration, and invasion, while enhancing apoptosis through modulation of the Hedgehog signaling pathway.

conclusionTIGD6 is overexpressed in GC and linked to unfavorable outcomes. It could potentially function as a biomarker and therapeutic target for this malignancy. Future studies should validate its clinical relevance and explore its detailed molecular mechanisms. Collectively, this study provides the first functional, mechanistic, and immune-phenotypic characterization of TIGD6 in GC, positioning it as a dual biomarker and therapeutic target.

Indexed as

Biomarkers, TumorIntracellular Signaling Peptides and ProteinsStomach NeoplasmsAgedCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedPrognosisBiomarkers, TumorIntracellular Signaling Peptides and ProteinsDrug sensitivityGastric cancerHedgehog signaling pathwayPrognosisTherapeutic targetTIGD6

Identifiers

PMID41121403
PMCPMC12538967

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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.