Y Xu1, Y-D Zhong, X-X Zhao. 1. Department of GI Medicine, Linyi Central Hospital, Linyi, China. 1293764732@qq.com.
Abstract
OBJECTIVE: This study aims to illustrate the role of microRNA-548 (miR-548) in regulating the development of colorectal cancer (CRC) and the involvement of WNT2. PATIENTS AND METHODS: MiR-548b levels in CRC species and paracancerous ones were detected. The relationship between miR-548b level and clinical parameters of CRC patients was analyzed. After overexpression of miR-548b, the changes in the proliferative and apoptotic capacities of Sw620 and HT29 cells were assessed by Cell Counting Kit-8 (CCK-8), colony formation assay, and flow cytometry, respectively. At last, the involvement of WNT2, the downstream gene of miR-548b, was detected by Luciferase assay and rescue experiments. RESULTS: Results manifested that miR-548b was lowly expressed in CRC species than paracancerous ones, and in vitro level of miR-548b was downregulated in CRC cell lines as well. Compared with CRC patients in T1-T2, miR-548b level was lower in T3-T4 CRC. Moreover, CRC patients with lymphatic metastasis had lower level of miR-548b than those without. Overexpression of miR-548b suppressed proliferative capacity and induced apoptosis in CRC cells. Besides, it was found that WNT2 was the downstream gene of miR-548b, and its level was negatively regulated by miR-548b in CRC. Furthermore, rescue experiments showed that WNT2 was responsible for CRC development regulated by miR-548b. CONCLUSIONS: MiR-548b is closely linked to tumor stage and lymphatic metastasis of CRC, and it alleviates the malignant development of CRC by targeting WNT2.
OBJECTIVE: This study aims to illustrate the role of microRNA-548 (miR-548) in regulating the development of colorectal cancer (CRC) and the involvement of WNT2. PATIENTS AND METHODS: MiR-548b levels in CRC species and paracancerous ones were detected. The relationship between miR-548b level and clinical parameters of CRC patients was analyzed. After overexpression of miR-548b, the changes in the proliferative and apoptotic capacities of Sw620 and HT29 cells were assessed by Cell Counting Kit-8 (CCK-8), colony formation assay, and flow cytometry, respectively. At last, the involvement of WNT2, the downstream gene of miR-548b, was detected by Luciferase assay and rescue experiments. RESULTS: Results manifested that miR-548b was lowly expressed in CRC species than paracancerous ones, and in vitro level of miR-548b was downregulated in CRC cell lines as well. Compared with CRC patients in T1-T2, miR-548b level was lower in T3-T4 CRC. Moreover, CRC patients with lymphatic metastasis had lower level of miR-548b than those without. Overexpression of miR-548b suppressed proliferative capacity and induced apoptosis in CRC cells. Besides, it was found that WNT2 was the downstream gene of miR-548b, and its level was negatively regulated by miR-548b in CRC. Furthermore, rescue experiments showed that WNT2 was responsible for CRC development regulated by miR-548b. CONCLUSIONS:MiR-548b is closely linked to tumor stage and lymphatic metastasis of CRC, and it alleviates the malignant development of CRC by targeting WNT2.