RETRACTED: DCLK1 promotes epithelial-mesenchymal transition via the PI3K/Akt/NF-κB pathway in colorectal cancer (Retracted Article)

被引:78
|
作者
Liu, Weiying
Wang, Shixing
Sun, Qi
Yang, Zhen
Liu, Min
Tang, Hua [1 ,2 ]
机构
[1] Tianjin Med Univ, Sch Basic Med Sci, Tianjin Life Sci Res Ctr, 22 Qi Xiang Tai Rd, Tianjin 300070, Peoples R China
[2] Tianjin Med Univ, Sch Basic Med Sci, Dept Pathogen Biol, 22 Qi Xiang Tai Rd, Tianjin 300070, Peoples R China
基金
中国国家自然科学基金; 中国博士后科学基金;
关键词
double cortin-like kinase 1; colorectal cancer; epithelial-mesenchymal transition; NF-kappa B; PI3K/Akt pathway; NF-KAPPA-B; STEM-CELL MARKER; VASCULOGENIC MIMICRY; EXPRESSION; TUMOR; GENE; TRANSCRIPTION; PHENOTYPE; BIOMARKER; PROTEIN;
D O I
10.1002/ijc.31232
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Double cortin-like kinase 1 (DCLK1) plays important roles during the epithelial-mesenchymal transition (EMT) process in human colorectal cancer (CRC). However, the role of DCLK1 in regulating the EMT of CRC is still poorly understood. In this study, we report evidence that DCLK1 acts as a potent oncogene to drive its extremely malignant character of EMT in an NF-kappa B-dependent manner in CRC cells. Mechanistic investigations showed that DCLK1 induced the NF-kappa Bp65 subunit expression through the PI3K/Akt/Sp1 axis and activated NF-kappa Bp65 through the PI3K/Akt/I kappa B alpha pathway during the EMT of CRC cells. Moreover, we found that silencing the expression of DCLK1 inhibited the invasion and metastasis of CRC cells in vivo. Collectively, our findings identify DCLK1 as a pivotal regulator of an EMT axis in CRC, thus implicating DCLK1 as a potential therapeutic target for CRC metastasis.
引用
收藏
页码:2068 / 2079
页数:12
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