ArticleJournal of gastroenterology2026
A PRK-armed oncolytic adenovirus drives calreticulin exposure for dendritic cell licensing to prime antitumor CD8⁺ T cells and synergizes with anti-PD-1 or CAR-T therapy in colorectal cancer.
Article in Journal of gastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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15 authors.
Funding
Abstract
backgroundThe therapeutic potential of oncolytic adenoviruses (ADVs) in colorectal cancer is constrained by a counterproductive host response: virus-triggered hyperactivation of the pro-survival AKT pathway, which fosters an immunosuppressive tumor microenvironment.
methodsWe engineered a novel oncolytic adenovirus, ADV-PRK, designed to co-express the AKT-inhibitory peptide PRK. Its antitumor efficacy and mechanisms were evaluated in syngeneic (MC38, CT26) and humanized mouse models. Molecular analyses (Western blot, immunofluorescence, and qPCR) elucidated signaling pathways. Immunological outcomes were assessed via flow cytometry and in vitro co-culture assays. Combination therapies with anti-PD-1 or CAR-T cells were tested in vivo.
resultsWe demonstrate that ADV-PRK abrogates phosphorylation of both AKT and its downstream effector, the ER calcium channel IP3R3. This suppression drives ER calcium efflux, inducing calreticulin (CRT) translocation to the cell surface. Surface-exposed CRT acts as a potent "eat-me" signal, licensing dendritic cells to prime and activate tumor-specific CD8⁺ T cells, which are essential for efficacy. In vivo, ADV-PRK monotherapy achieved superior tumor control. It demonstrated potent synergy with both anti-PD-1 and CAR-T cell therapy, by remodeling the immune landscape to expand activatable T cells and support adoptive cellular therapy. Its activity in a humanized model confirms translational relevance.
conclusionsOur work delineates a distinct immunomodulatory axis, AKT-IP3R3-Ca
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