ZNF184-mediated transcriptional activation of SAE1 drives the cell cycle entry and immune evasion in non-small cell lung cancer.
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ABSTRACT: Non-small cell lung cancer (NSCLC) is a highly prevalent subtype of lung cancer with an unsatisfactory prognosis, necessitating new therapeutic targets. The ubiquitin-like SUMO proteins covalently modify substrates and their functional properties. Here we report that SAE1 regulates p53 signaling through its ability to SUMOylate p53 and dissect the upstream modifiers of SAE1. Basal SAE1 levels were elevated in NSCLC cells, especially lung adenocarcinoma A549 and squamous cell carcinoma PC-10 lines. To probe SAE1 function, we utilized lentiviral short hairpin RNAs to stably knock down SAE1 in A549 and PC-10 cells. Knockdown of SAE1 significantly impeded the immune invasion in NSCLC in vitro and in vivo and promoted cell cycle arrest of NSCLC cells in vitro. Mechanistically, SAE1 knockdown su
SUBMITTER: Shi F
PROVIDER: S-EPMC12481743 | biostudies-literature | 2025 Sep
REPOSITORIES: biostudies-literature
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