Hu Fengqing, Tao Zhen, Wang Mingsong, Li Guoqing, Zhang Yunjiao, Zhong Hong, Xiao Haibo, Xie Xiao, Ju Mei
Department of Cardiothoracic Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Rd, Shanghai, 200092, China.
Tumour Biol. 2013 Dec;34(6):3893-9. doi: 10.1007/s13277-013-0977-7. Epub 2013 Jul 27.
Dysregulation of hedgehog signaling has been involved in esophageal squamous cell carcinoma (ESCC) by the mechanisms that are not fully understood. The receptor for activated protein kinase C (RACK1) is involved in the progression of multiple cancers. However, its expression and function in ESCC have not been investigated. Here, we found that the expression of RACK1 was upregulated in ESCC clinical samples. Moreover, over-expression of RACK1 in ESCC cells promoted cell proliferation and migration, while downregulation of RACK1 impaired the proliferation and migration of ESCC cells in vitro and in vivo. Mechanistically, RACK1 promoted the proliferation and migration of ESCC cells by activating hedgehog signaling. Taken together, our study suggested RACK1 might be an important therapeutic target in ESCC.
刺猬信号通路的失调通过尚未完全了解的机制参与了食管鳞状细胞癌（ESCC）的发生发展。活化蛋白激酶C受体（RACK1）参与多种癌症的进展。然而，其在ESCC中的表达和功能尚未得到研究。在此，我们发现RACK1在ESCC临床样本中的表达上调。此外，ESCC细胞中RACK1的过表达促进细胞增殖和迁移，而RACK1的下调则在体外和体内损害ESCC细胞的增殖和迁移。机制上，RACK1通过激活刺猬信号通路促进ESCC细胞的增殖和迁移。综上所述，我们的研究表明RACK1可能是ESCC的一个重要治疗靶点。
