Evidence map›Paper›PMID 42010588›Full record

ArticleWorld journal of surgical oncology2026

RGS19 drives tumor progression and immunosuppression in clear cell renal cell carcinoma by modulating CAMs and EMT.

Zhenhui Li, Zhusheng Lian, Kuo Ma, Weihang Song, Xiangdong Xue, Lei Li

Abstract read
In one paragraph

Article in World journal of surgical oncology, 2026. 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

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Zhenhui LiDepartment of Urology, the First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China. 15136193707@163.com.
Zhusheng LianDepartment of Radiation Oncology, the First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Kuo MaDepartment of Urology, the First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Weihang SongDepartment of Urology, the First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Xiangdong XueDepartment of Urology, the First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Lei LiDepartment of Urology, the First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenal cell carcinoma (RCC) is characterized by poor prognosis and limited treatment options.This study aims to characterize the clinical significance, biological functions, and underlying mechanisms of RGS19 in clear cell renal cell carcinoma (ccRCC) and preliminarily analyze its association with the tumor immune microenvironment.

methodsThe expression pattern of RGS19 was analyzed using TCGA datasets, GEO databases, and clinical specimens. Its biological functions were verified through in vitro assays and in vivo experimental models. Correlations between RGS19 and cell adhesion molecules (CAMs), epithelial-mesenchymal transition (EMT)-related genes, and signaling pathways were analyzed. Immune infiltration analysis was also performed to explore the association between RGS19 expression and tumor immune microenvironment.

resultsRGS19 was markedly elevated in ccRCC tissues and cell lines compared with normal control groups. Its elevated expression correlated with advanced TNM stage, higher histologic grade, and poorer overall, progression-free, and disease-specific survival, establishing it as an independent prognostic factor. Furthermore, functional assays confirmed that RGS19 depletion curbed ccRCC cell proliferation, migration, and invasion in vitro, and attenuated tumor growth in xenograft models. RGS19 overexpression exerted the opposite effects. RGS19 was positively correlated with CAMs and EMT-related genes, and enriched in cell adhesion and EMT signaling pathways. Furthermore, expression of RGS19 was associated with increased infiltration of immunosuppressive cell populations and diminished infiltration of Th17 cell subsets.

conclusionRGS19 promotes ccRCC progression through CAM-mediated adhesion, EMT, and immunosuppression, suggesting its clinical utility as a prognostic marker and a promising target for therapy.

Indexed as

Biomarkers, TumorCarcinoma, Renal CellCell Adhesion MoleculesEpithelial-Mesenchymal TransitionKidney NeoplasmsRGS ProteinsAnimalsCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMiddle AgedBiomarkers, TumorCell Adhesion MoleculesRGS ProteinsCell adhesion moleculesClear cell renal cell carcinomaEpithelial-mesenchymal transitionPrognostic biomarkerRGS19

Identifiers

PMID42010588
PMCPMC13227676

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.