SYT7 accelerates nasopharyngeal carcinoma progression via ALDH1A3-mediated STAT3 signaling activation.

ABSTRACT: Nasopharyngeal carcinoma (NPC) is a special histological and ethical type of head and neck cancer with unsatisfactory clinical outcome. Thus, exploring effective molecular targets is critical for NPC treatment. We observed increased expression levels of synaptotagmin-7 (SYT7) in NPC tissues, which correlated with unfavorable prognoses. Furthermore, knockdown of SYT7 in NPC cells suppressed proliferation and migration rates, and enhanced apoptosis. In contrast, overexpression of SYT7 accelerated NPC tumor growth. Using whole-genome gene arrays and immunoprecipitation-mass spectrometry assays, aldehyde dehydrogenase 1 family member A3 (ALDH1A3), a regulator of glycolytic metabolism, was identified as a critical downstream target of SYT7. Mechanistically, SYT7 binds and promotes ALDH1A3 deubi

SUBMITTER: Xu K 

PROVIDER: S-EPMC12064795 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature