Claudin-14 promotes colorectal cancer progression via the PI3K/AKT/mTOR pathway

被引:17
|
作者
Qiao, Tian-Yu [1 ]
Yuan, Zi-Ming [1 ]
Ma, Tian-Yi [1 ]
Hu, Han-Qing [1 ]
Zhu, Yi-Hao [1 ]
Zhang, Wei-Yuan [1 ]
Zhang, Qian [1 ]
Huang, Rui [1 ]
Tang, Qing-Chao [1 ]
Wang, Gui-Yu [2 ]
Wang, Xi-Shan [1 ,3 ]
机构
[1] Harbin Med Univ, Dept Colorectal Surg, Affiliated Hosp 2, Harbin, Peoples R China
[2] Univ Chinese Acad Sci, Dept Colorectal Surg, Canc Hosp, Hangzhou, Peoples R China
[3] Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp, Natl Canc Ctr, Natl Clin Res Ctr Canc, Beijing, Peoples R China
关键词
colorectal cancer; Claudin-14; PI3K/AKT/mTOR pathway; SIGNALING PATHWAY; BIOMARKER; CLDN14;
D O I
10.4149/neo_2021_210210N203
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Colorectal cancer is the third leading cancer in the world in terms of incidence and mortality. The role of differentially expressed Claudin-14 (CLDN14) in CRC has not been reported. We observed that CLDN14 was associated with the progression of CRC. Our functional studies have shown that CLDN14 promoted the proliferation of CRC cells. In addition, CLDN14 also increased the migration and invasion of CRC cells. In vivo experiments also showed that CLDN14 promoted the growth of colorectal cancer via the PI3K/AKT/mTOR. In summary, our research suggests that CLDN14 promotes the progression of colorectal cancer. Our findings may provide new strategies for clinical management and patient prognosis of CRC.
引用
收藏
页码:947 / +
页数:9
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