ArticleCancer genomics & proteomics
ATIC Knockdown Reduces B7-H3 Expression and Oncogenic Signaling in Upper Tract Urothelial Carcinoma Cells.
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Reprogramming-driven Proteomic Shifts Mirror Bladder Cancer Progression and Reveal Biomarker Candidates Across Disease Grades.Cancer genomics & proteomicsArticle
- Integrated Immunotherapy Target Atlas for Ewing Sarcoma.Cancer genomics & proteomicsReview
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimUpper tract urothelial carcinoma (UTUC) has a notably high incidence and aggressiveness in East Asian populations; however, its molecular mechanisms remain poorly defined. Our previous study identified 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase (ATIC), a bifunctional enzyme involved in MATERIALS AND
methodsTo elucidate ATIC-regulated signaling pathways, we performed tandem mass tag (TMT)-based quantitative proteomics in BFTC909 cells with ATIC knockdown, followed by functional, biochemical, and drug-sensitivity assays.
resultsProteomic profiling identified B7-H3 (CD276), prion protein (PRNP), RAC2, and NT5E (CD73) as downstream molecules downregulated by ATIC silencing. Functional assays revealed that suppressing the expression of these proteins inhibited cell proliferation, migration, and invasion, and enhanced cisplatin sensitivity. RNA interference analysis indicated that B7-H3 may lie upstream of prion protein and RAC2. Mechanistically, the ATIC/B7-H3 axis were shown to modulate mTOR, AKT, ERK, and p38 phosphorylation, linking metabolic activity to oncogenic and chemoresistant signaling.
conclusionThese findings revealed an ATIC-associated metabolic-immunoregulatory network in UTUC, through which ATIC supports mTOR-related signaling and promotes tumor progression and cisplatin resistance. Targeting the ATIC-driven network may offer new therapeutic opportunities for UTUC management.
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