ArticleJournal of translational medicine2026
Cathepsin E drives colorectal cancer progression and immune evasion via ZNF326 ADP-ribosylation and TGF-β/SMAD activation.
Article in Journal of translational medicine, 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
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Who cites it
1 citing paper in PubMed.
- Cathepsins as Core Players in Obesity Pathogenesis: Emerging Therapeutic Targets.Biomolecules · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal cancer (CRC) is a leading malignant tumor worldwide with rising morbidity and mortality. Cathepsin E (CTSE), a member of the cysteinyl asparaginase family, is implicated in immune responses, antigen processing, and cellular signaling.
methodsThe biological functions of CTSE in CRC were assessed through in vitro and in vivo experiments evaluating proliferation, invasion, and metastasis. Mechanistic studies utilized knockdown approaches, pathway inhibition, and analysis of post-translational modifications to investigate CTSE-mediated ADP-ribosylation. The impact of CTSE on tumor immunity was examined by analyzing PD-L1/PD-1 interactions and CD8
resultsCTSE promoted CRC proliferation, invasion, metastasis, and immune escape. Mechanistically, CTSE stabilized ZNF326 by promoting its ADP-ribosylation at glutamate 338, thereby activating TGF-β/SMAD pathway. The tumor-promoting effect was abolished by ZNF326 knockdown or TGF-β/SMAD pathway inhibition. Furthermore, CTSE enhanced PD-L1/PD-1 interactions and reduced secretion of anti-tumor factors, thereby impairing CD8
conclusionsCTSE drives CRC progression by stabilizing ZNF326 via ADP-ribosylation and activating TGF-β/SMAD pathway, while facilitating tumor immune evasion. CTSE represents a promising therapeutic target for CRC, and its combination with PD-1/PD-L1 inhibitors may synergistically enhance anti-tumor efficacy.
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