ArticleCell death & disease2026
Endoplasmic reticulum stress-induced histone lactylation mediating immune escape of gastric cancer via PDIA6 overexpression in dendritic cells.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Lactate metabolism and protein lactylation in inflammatory and tumor microenvironments.Molecular biomedicine · 2026Review
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8 authors.
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Abstract
Gastric cancer is one of the most prevalent cancers worldwide and is associated with a high mortality rate. Although immunotherapy has achieved some success for many tumor types, the limited response of gastric cancer to immunotherapy poses a challenge. Lactylation is a recently proposed post-translational modification derived from lactate that plays a key role in many physiological processes. In this study, we found that endoplasmic reticulum stress (ERS)-induced histone lactylation attenuated the immune response of dendritic cells (DC), decreased the ability of T cells to kill tumor cells, and enhanced tumor growth. Interestingly, ERS-induced H4K12 lactylation promoted the expression of PDIA6 in DC, leading to weakened immune activity of DC and decreased anti-tumor ability of T cells, thereby promoting gastric cancer immune evasion. Collectively, our work provides new insights into how ERS-induced lactylation modification attenuates the stability of DC to drive immune escape in gastric cancer and provides a promising biomarker for the efficacy of immunotherapy in gastric cancer.
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