当归素通过负向调节双特异性磷酸酶6/原癌基因c-MYC信号通路抑制口腔鳞状细胞癌的细胞生长并促进其凋亡。
Angelicin inhibits cell growth and promotes apoptosis in oral squamous cell carcinoma by negatively regulating DUSP6/cMYC signaling pathway.
作者信息
Liu Na, Li Chunyu, Shang Qianhui, Qi Jiajia, Li Qionghua, Deng Jing, Dan Hongxia, Xie Liang, Chen Qianming
机构信息
State Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan, China; Department of Periodontics, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangdong Engineering Research Center of Oral Restoration and Reconstruction, Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou 510182, China.
State Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan, China.
出版信息
Exp Cell Res. 2023 Nov 15;432(2):113793. doi: 10.1016/j.yexcr.2023.113793. Epub 2023 Sep 21.
Angelicin has been reported to have antitumor effects on many types of cancer. However, few studies on angelicin in oral squamous cell carcinoma (OSCC) have been performed. We performed cell cycle and apoptosis analyses to assess the effect of angelicin on OSCC cells. We conducted RNA-seq studies to reveal differentially expressed genes (DEGs). Dual-specificity phosphatase 6 (DUSP6) and c-MYC were strongly down-regulated differential genes. Silencing RNA (siRNA) was used to knockdown DUSP6. The mouse xenograft model was used to mimic OSCC. Angelicin inhibited OSCC in vitro. We found that DUSP6 interacted with c-MYC. DUSP6 knockdown group and DUSP6 knockdown + angelicin group had similar effects of OSCC cells. Angelicin could reduce tumor formation, DUSP6, and c-MYC expression in vivo. Compared with paclitaxel, the tumor inhibition effect of the two drugs was similar. However, angelicin did not cause weight loss and had lower toxicity. In sum, Angelicin has antitumor effects on OSCC in vitro and vivo by negatively regulating the DUSP6 mediated c-MYC signaling pathway.
据报道，当归素对多种癌症具有抗肿瘤作用。然而，关于当归素在口腔鳞状细胞癌（OSCC）方面的研究却很少。我们进行了细胞周期和凋亡分析，以评估当归素对OSCC细胞的影响。我们开展了RNA测序研究，以揭示差异表达基因（DEG）。双特异性磷酸酶6（DUSP6）和c-MYC是强烈下调的差异基因。使用小干扰RNA（siRNA）敲低DUSP6。利用小鼠异种移植模型模拟OSCC。当归素在体外抑制OSCC。我们发现DUSP6与c-MYC相互作用。DUSP6敲低组和DUSP6敲低+当归素组对OSCC细胞的作用相似。当归素在体内可减少肿瘤形成、DUSP6和c-MYC的表达。与紫杉醇相比，两种药物的肿瘤抑制效果相似。然而，当归素不会导致体重减轻，且毒性较低。总之，当归素通过负向调节DUSP6介导的c-MYC信号通路，在体外和体内对OSCC均具有抗肿瘤作用。
Zotero 插件