MicroRNA-302a enhances 5-fluorouracil-induced cell death in human colon cancer cells

被引:34
作者
Liu, Na [1 ]
Li, Jie [2 ]
Zhao, Zhenghao [1 ]
Han, Jia [1 ]
Jiang, Ting [1 ]
Chen, Yanke [1 ]
Hou, Ni [1 ]
Huang, Chen [1 ,3 ]
机构
[1] Xi An Jiao Tong Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Cell Biol & Genet, 76 Western Yanta Rd, Xian 710061, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Hlth Sci Ctr, Affiliated Hosp 2, Dept Gen Surg, Xian 710061, Shaanxi, Peoples R China
[3] Xi An Jiao Tong Univ, Hlth Sci Ctr, Key Lab Environmentally & Genetically Associated, Xian 710061, Shaanxi, Peoples R China
基金
中国国家自然科学基金;
关键词
microRNA-302a; insulin-like growth factor-1 receptor; 5-fluorouracil; Akt; human colon cancer cell; FACTOR-I-RECEPTOR; COLORECTAL-CANCER; MAMMALIAN TARGET; TUMOR-GROWTH; STEM-CELLS; RESISTANCE; CARCINOMA; CHEMOSENSITIVITY; CHEMOTHERAPY; SENSITIVITY;
D O I
10.3892/or.2016.5237
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
New therapeutic strategies are needed for colorectal cancer (CRC) treatment. MicroRNAs are involved in cancer-pertinent cellular processes, including chemoresistance. As miR-302a is an embryonic stem cell-specific microRNA, studies on miR-302a have focused on its role in human stem cells. Studies analyzing miR-302 function in cancer are limited. In this study, we used two human colon cancer cell lines, HCT116 and HT29, and evaluated the influence of miR-302a on 5-fluorouracil (5-FU)-induced cell death and viability inhibition. With bioinformatics tools, we hypothesized that insulin-like growth factor-1 receptor (IGF-1R) is a novel target of miR-302a, which we confirmed using a luciferase reporter assay and immunoblotting. Then, we designed siRNA against IGF-1R and found that si-IGF-1R resembled the effect of miR-302a on 5-FU treatment. Both miR-302a and si-IGF-1R inhibited Akt signaling. In conclusion, miR-302a targeted IGF-1R and enhanced 5-FU-induced cell death and viability inhibition in human colon cancer cells. Targeting miR-302a may offer new therapeutic interventions in CRC.
引用
收藏
页码:631 / 639
页数:9
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