Na Su1, Li Liu2, Shan He1, Linghai Zeng3. 1. Department of Clinical Laboratory, The First People's Hospital of Jingmen, No. 67 Xiangshan Avenue, Jingmen, 448000, Hubei, China. 2. Department of Nephropathy, Jingmen No. 2 People's Hospital, Jingmen, Hubei, China. 3. Department of Clinical Laboratory, The First People's Hospital of Jingmen, No. 67 Xiangshan Avenue, Jingmen, 448000, Hubei, China. glbxrw@163.com.
Abstract
BACKGROUND: Circular RNAs (circRNAs) play important roles in the progression of various cancers, including breast cancer (BC). However, the role of circ_0001666 in BC remains unclear. OBJECTIVE: To explore the role of circ_0001666 in the progression of BC and reveal its potential molecular mechanism. METHODS: Real-time polymerase chain reaction was conducted to determine the expression of circ_0001666, miR-620 and with-no-lysine kinase 2 (WNK2). Cell counting kit 8 assay, flow cytometry and transwell assay were used to measure cell proliferation, apoptosis, migration and invasion. Western blot was utilized to examine the level of protein. Dual-luciferase reporter assay and RNA immunoprecipitation assay were used to verify the interaction between miR-620 and circ_0001666 or WNK2. Mice xenotransplantation models were built to explore the effect of circ_0001666 on BC tumor growth in vivo. RESULTS: Circ_0001666 was downregulated in BC tumor tissues and cells. Overexpressed circ_0001666 inhibited the proliferation, migration, invasion, while promoted apoptosis and tumor growth of BC in vitro or in vivo. Furthermore, circ_0001666 could serve as a sponge of miR-620. MiR-620 inhibitor hindered BC cell progression, which was similar to the effect of circ_0001666 overexpression. WNK2 was a target of miR-620, and circ_0001666 could sponge miR-620 to positive regulate WNK2. The knockdown of WNK2 reversed the effect of circ_0001666 overexpression on BC progression. CONCLUSION: Circ_0001666 hindered the progression of BC via miR-620/WNK2 axis.
BACKGROUND: Circular RNAs (circRNAs) play important roles in the progression of various cancers, including breast cancer (BC). However, the role of circ_0001666 in BC remains unclear. OBJECTIVE: To explore the role of circ_0001666 in the progression of BC and reveal its potential molecular mechanism. METHODS: Real-time polymerase chain reaction was conducted to determine the expression of circ_0001666, miR-620 and with-no-lysine kinase 2 (WNK2). Cell counting kit 8 assay, flow cytometry and transwell assay were used to measure cell proliferation, apoptosis, migration and invasion. Western blot was utilized to examine the level of protein. Dual-luciferase reporter assay and RNA immunoprecipitation assay were used to verify the interaction between miR-620 and circ_0001666 or WNK2. Mice xenotransplantation models were built to explore the effect of circ_0001666 on BC tumor growth in vivo. RESULTS: Circ_0001666 was downregulated in BC tumor tissues and cells. Overexpressed circ_0001666 inhibited the proliferation, migration, invasion, while promoted apoptosis and tumor growth of BC in vitro or in vivo. Furthermore, circ_0001666 could serve as a sponge of miR-620. MiR-620 inhibitor hindered BC cell progression, which was similar to the effect of circ_0001666 overexpression. WNK2 was a target of miR-620, and circ_0001666 could sponge miR-620 to positive regulate WNK2. The knockdown of WNK2 reversed the effect of circ_0001666 overexpression on BC progression. CONCLUSION: Circ_0001666 hindered the progression of BC via miR-620/WNK2 axis.