ArticleJournal of thoracic disease2025
ST6GALNAC1 mediates sialylation of mucins in non-small cell lung cancer to evade immune surveillance.
Article in Journal of thoracic disease, 2025. 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.
- Aberrant sialylation in cancer: From molecular mechanisms to potential therapeutics.Genes & diseases · 2026Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Non-small cell lung cancer (NSCLC) ranks first among common cancers worldwide and first among causes of cancer death. This study explored the function of ST6 N-acetylgalactosaminide alpha-2,6-sialyltransferase 1 (ST6GALNAC1) on immune surveillance in NSCLC. Methods: All the samples (patients with NSCLCs) were immediately snap frozen in liquid nitrogen and stored at -80 ℃ for further using. Mice were randomly divided into two groups. And functional verification was performed in combination with quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay, western blot, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) proliferation assay and transwell co-culture system. Results: We found that ST6GALNAC1 expression in patients with NSCLC were up-regulated. Overall survival (OS) and disease-free survival (DFS) of patients with ST6GALNAC1 up-regulation were lower than those of patients with ST6GALNAC1 down-regulation. In mice model of NSCLC, ST6GALNAC1 promoted cancer cell growth and immune surveillance. ST6GALNAC1 promoted the invasion and migration of NSCLCs. ST6GALNAC1 promotes ferroptosis of macrophage. ST6GALNAC1 suppressed p-Akt expression of macrophage to promote ferroptosis of macrophage. Akt agonists reduced the effects of ST6GALNAC1 on immune surveillance. Conclusions: Together, these results show that ST6GALNAC1 evades immune surveillance in NSCLC by Akt, suggesting that targeting ST6GALNAC1 may reduce ferroptosis of macrophage in NSCLCs. This infers that ST6GALNAC1 is potential target to be used in the treatment of NSCLCs.
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