ArticleOncogene2026
The YY1-KIF15-PRDX1 axis promotes gastric cancer progression by inducing mitochondrial ROS imbalance.
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Gastric cancer (GC) remains a leading cause of global cancer mortality, necessitating deeper molecular insights. This study identifies KIF15 as a key driver of GC progression through integrated analysis of TCGA data and experimental validation. KIF15 is significantly overexpressed in GC tissues and correlates with advanced tumor stage, metastasis, and poor prognosis. Functional assays demonstrate that KIF15 enhances cancer stem cell (CSC) properties, proliferation, migration, invasion, and cisplatin resistance in GC cells. Mechanistically, KIF15 interacts with peroxiredoxin 1 (PRDX1), stabilizing this antioxidant protein to reduce intracellular hydroperoxides and maintain mitochondrial function. Depletion of PRDX1 reverses KIF15-mediated oncogenic effects. Further investigation reveals Yin Yang 1 (YY1) as the upstream transcriptional activator of KIF15. YY1 directly binds the KIF15 promoter, and its overexpression elevates KIF15 expression. Rescue experiments confirm that YY1 promotes GC malignancy via the KIF15-PRDX1 axis. Crucially, YY1 also transcriptionally regulates PRDX1, forming a coordinated regulatory circuit. In vivo models corroborate that the YY1/KIF15/PRDX1 axis drives tumor growth, metastasis, and chemoresistance. Collectively, these findings establish a novel YY1-KIF15-PRDX1 signaling axis that induces mitochondrial ROS imbalance to facilitate GC progression, offering potential prognostic markers and therapeutic targets.
Indexed as
Identifiers
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Registered trials
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.