ReviewFrontiers in oncology2025
CHAC1 in urological tumors: contextual dualism and therapeutic implications.
Review in Frontiers in oncology, 2025. 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.
- GSH-Related Enzymes GPx4, Chac1, and GSTs and Redox Regulation of Ferroptosis in Cancer.International journal of molecular sciences · 2026Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CHAC1, a glutathione-degrading enzyme, governs context-dependent pathophysiological processes in urological malignancies through modulation of endoplasmic reticulum stress and ferroptotic pathways. In clear cell renal cell carcinoma (ccRCC), CHAC1 exhibits stage-specific functional duality: downregulation in early-stage tumors correlates with adverse prognosis (suggesting tumor-suppressive activity), whereas elevated expression in advanced ccRCC (G3-G4/Stage III-IV) associates with increased mortality (indicating adaptive pro-survival adaptation). For prostate cancer, CHAC1 potentiates docetaxel cytotoxicity via coordinated induction of endoplasmic reticulum stress and ferroptosis, yet its suppression by cancer-associated fibroblast-derived exosomal miR-432-5p establishes therapy-reinforced chemoresistance. Mechanistically, CHAC1 intersects critical pathways by regulating redox homeostasis through glutathione catabolism, mediating potential crosstalk with androgen receptor signaling, and serving as an independent prognostic determinant in ccRCC (FPTOS_score model: HR = 2.028, 95% CI: 1.640-2.507). Notably, current evidence reveals no established link between CHAC1 and urothelial carcinoma pathogenesis. Further elucidation of CHAC1's mechanistic intricacies and therapeutic targeting (e.g., CHAC1 agonists, exosomal miRNA antagonists) may advance precision management of urological tumors.
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