E3泛素连接酶RNF126调控舌癌进展。

Wang Lina, Wang Xin, Zhao Yuehan, Niu Weidong, Ma Guowu, Yin Wei, Shi Chun

Department of Endodontics, College of Stomatology, Dalian Medical University, Dalian, 116044, China.

The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, 430072, China.

Cancer Med. 2016 Aug;5(8):2043-7. doi: 10.1002/cam4.771. Epub 2016 May 26.

This study aims to analyze the role of RNF126 in the oncogenesis of tongue cancer. The cell proliferation and viability of human tongue cancer cells, SCC25 and SCC9 cells, were determined by cell counting and MTT assay, respectively. The effect of RNF126 on regulating AKT signaling pathway was analyzed through western blotting. The transplantation tumor model of nude mice was used to evaluate the tumorigenecity of RNF126. Knockdown of RNF126 inhibited the proliferation and viability of SCC9 and SCC25 cells. Inhibition of RNF126 also decreased the activity of AKT1 as well as its downstream molecules. Furthermore, RNF126 regulated the tumor volume on mice model. These data suggested that RNF126 might be related to the progression of tongue cancer through regulating AKT signaling pathway.

本研究旨在分析RNF126在舌癌发生过程中的作用。分别通过细胞计数和MTT法测定人舌癌细胞SCC25和SCC9细胞的增殖和活力。通过蛋白质免疫印迹法分析RNF126对AKT信号通路的调节作用。利用裸鼠移植瘤模型评估RNF126的致瘤性。敲低RNF126可抑制SCC9和SCC25细胞的增殖和活力。抑制RNF126也降低了AKT1及其下游分子的活性。此外，RNF126调节小鼠模型中的肿瘤体积。这些数据表明，RNF126可能通过调节AKT信号通路与舌癌的进展有关。