ArticleAmerican journal of cancer research2026
DDOST mediates cervical cancer cell malignant progression by interacting with SMARCA4.
Article in American journal of cancer research, 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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Abstract
DDOST is generally recognized as a regulator of glycosylation homeostasis and its deficiency can cause congenital glycosylation disorders. However, its role in tumors has not yet been elucidated. This study aimed to explore the functional role of DDOST and its related mechanisms in cervical cancer (CC). The clinical correlation of DDOST was analyzed using The Cancer Genome Atlas (TCGA) database and verified by immunohistochemistry slides of clinical samples. Cell growth, proliferation, apoptosis, migration, and invasion were evaluated. Co-immunoprecipitation (co-IP) and liquid chromatography with tandem mass spectrometry (LC-MS) were used to identify interacting proteins. The functions of the interacting proteins were further confirmed using genetic rescue experiments. A subcutaneous xenograft model was used to investigate tumorigenesis. Based on the TCGA data and our collected clinical samples, we found that DDOST was associated with a more aggressive pathological phenotype. DDOST also promoted several malignant phenotypes in CC cells. Co-IP coupled with LC-MS identified the interacting protein SMARCA4, and western blotting confirmed a positive interaction between these two proteins. Similar to in vivo tumorigenesis, cell growth and migration were markedly rescued by SMARCA4 overexpression after DDOST knockdown, as was tumorigenesis
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