LGR5 promotes the proliferation of colorectal cancer cells via the Wnt/β-catenin signaling pathway

被引:35
作者
Lin, Yu [1 ,2 ]
Wu, Tingyu [1 ]
Yao, Qianqian [1 ]
Zi, Shuming [1 ]
Cui, Long [1 ,3 ]
Yang, Ming [1 ]
Li, Jinming [1 ,3 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp Affiliated, Dept Colorectal Surg, Shanghai 200092, Peoples R China
[2] Fujian Med Univ, Union Hosp, Dept Colorectal Surg, Fuzhou 350001, Fujian, Peoples R China
[3] Shanghai Jiao Tong Univ, Sch Med, Shanghai Colorectal Canc Res Ctr, Shanghai 200092, Peoples R China
关键词
colorectal cancer; leucine-rich repeat-containing G-protein coupled receptor 5; Wnt/beta-catenin signaling; small interfering RNA; PROTEIN-COUPLED RECEPTOR; STEM-CELLS; BETA-CATENIN; COLON-CANCER; WNT RECEPTORS; OVEREXPRESSION; IDENTIFICATION; GPR49; INTESTINE; CARCINOMA;
D O I
10.3892/ol.2015.3144
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5) is an established cancer stem cell marker and is a target gene of the Wnt/beta-catenin signaling pathway, a critical pathway in the process of tumor initiation and growth. In the present study, the mRNA expression levels of LGR5, adenomatous polyposis coli (APC) and beta-catenin were detected in 20 colorectal cancer (CRC) tissues and matched healthy mucosa samples using reverse transcription-quantitative polymerase chain reaction. HT-29 CRC cell line was treated with siRNA-Lgr5; the APC, beta-catenin and LGR5 RNA expressions were detected and cell viability was measured using a CCK8 assay. The results revealed that LGR5 was significantly overexpressed in CRC tissue compared with healthy mucosa (P<0.05). Furthermore, knockdown of LGR5 by small interfering RNA decreased the expression of APC and (3-catenin in HT29 colon cancer cells as well as inhibited the proliferation of HT29 cells. These findings demonstrated that LGR5 expression is critical for the promotion of neoplastic CRC cell proliferation, indicating that LGR5 may be a novel therapeutic target for CRC.
引用
收藏
页码:2859 / 2863
页数:5
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