The role and mechanism of circadian clock gene BMAL1 in the proliferation and metastasis of nasopharyngeal carcinoma by inhibition TGF-β1/Smads pathway.

• DOI: 10.1200/jco.2024.42.16_suppl.6027
• Publication Date: 2024-06-10T16:19:15Z
• Authors: Zhao Chaofen; Feng Jin; Lina Liu; Qianyong He; Yue Chen; Kai Shang; Xiaomei Li; Xinyu Xu; Xunyan Luo
• Keywords: 03 medical and health sciences; 0302 clinical medicine

6027 Background: To explore the molecular mechanism of biological clock gene BMAL1 inhibiting proliferation and metastasis nasopharyngeal carcinoma(NPC). Methods: 1. IHC detected expression in 41 cases chronic inflammatory tissue 71 NPCtissue. PCR Western blot measured levels NP69 NPC cells human immortalized epithelial cells, respectively. 2. detect effect on capacity NPCcells vitro vivo; Scratch healing Transwell invasion migration experiments ability vitro. Fluorescence vivo imaging HE staining to determine transfer nude mouse tail intravenous injection model. EMT-related markers at transcriptional protein cells. 3. A series means such as bioinformatics technology, ChIP experiment, double luciferase reporter immunofluorescence colocalization experiment Co-IP were used verify its mechanism. Results: The NPCtissues is reduced. tissues was associated with M stage carcinoma patients (p=0.006). Overexpression can inhibit proliferation, cancer while knocking down opposite. inhibits EMT NPCcells. There are 5 binding sites TGF-β1promoter region, directly bind which activity TGF-β1. TGF-β1/Smads pathway activity. Under induction recombinant TGF-β1, enhanced, signaling underwent EMT, cell increased. After overexpression BMAL1, TGF-β1 no longer promotes activity, inhibited, weakened. combined has certain diagnostic value predicting whether metastasis. Conclusions: downregulated carcinoma, level related development carcinoma. epithelial-mesenchymal transformation inhibition It speculated that it may become a new prognostic marker therapeutic target for