ArticlePloS one2025
RETRACTED: SPAG6 hypermethylation silences a novel tumor suppressor and inhibits renal cell carcinoma progression via PI3K/AKT/mTOR pathway.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Article
- Article
Corrections and comments
- Correction · 2026-03-13Error in Text · Updated to Retraction ·
- Retraction · 2026-05-22Concerns/Issues about Article · Concerns/Issues about Results and/or Conclusions · Objections by Author(s) · Upgrade/Update of Prior Notice(s) ·
- Erratum issued
- Retracted
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRenal cell carcinoma (RCC) ranks among the most prevalent malignancies of the genitourinary system, with a steadily rising incidence. Despite growing attention, the etiology and underlying mechanisms of RCC remain incompletely understood. Epigenetic modifications, particularly DNA methylation, have emerged as critical regulators in various malignancies, including RCC. Sperm-associated antigen 6 (SPAG6), initially identified in human testicular tissue and considered a marker for testicular tumors, has been associated with the pathophysiology of several malignancies. This study aimed to elucidate the role of aberrant SPAG6 methylation in RCC progression.
methodsWe first analyzed SPAG6 expression and methylation patterns in RCC and adjacent normal tissues using data from The Cancer Genome Atlas (TCGA) and the Epigenome-Wide Association Study (EWAS) databases. Clinical tissue specimens from Peking University First Hospital were then examined to explore the association between SPAG6 expression/methylation and the clinicopathological features of RCC patients. The correlation between SPAG6 expression and promoter methylation was further validated in RCC cell lines. Functional roles of SPAG6 in cell proliferation, invasion, cell cycle regulation, and apoptosis were investigated through in vitro cellular assays and in vivo xenograft models. Finally, transcriptome sequencing was performed to explore the molecular mechanisms by which SPAG6 affects RCC development.
resultsSPAG6 expression was markedly downregulated in RCC tissues compared to adjacent non-tumorous counterparts, because of promoter CpG hypermethylation. SPAG6 expression was associated with tumor stage in RCC patients. Functional assays demonstrated that SPAG6 suppresses RCC cell proliferation, invasion, and cell cycle progression, while promoting apoptosis. Mechanistically, SPAG6 inhibited RCC progression by negatively regulating the PI3K/AKT/mTOR signaling pathway.
conclusionsSPAG6 functions as a tumor suppressor in RCC, with its silencing driven by promoter hypermethylation. Through modulation of the PI3K/AKT/mTOR pathway, SPAG6 plays a vital role in restraining RCC initiation and progression.
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