Guohua Gong1,2, Jikai She1,3, Danni Fu1,3, Dong Zhen1,3, Bin Zhang1,2. 1. Inner Mongolia Key Laboratory of Mongolian Medicine Pharmacology for Cardio-Cerebral Vascular System Tongliao, Inner Mongolia Autonomous Region, China. 2. First Clinical Medical of Inner Mongolia University for Nationalities Tongliao, Inner Mongolia Autonomous Region, China. 3. Medicinal Chemistry and Pharmacology Institute, Inner Mongolia University for The Nationalities Tongliao, Inner Mongolia Autonomous Region, China.
Abstract
OBJECTIVE: We aimed to investigate the mechanism of circular RNA circ_0084927 in the progression of breast cancer (BC). METHODS: The levels of circ_0084927, miR-142-3p, and ELKS/RAB6-interacting/CAST family member-1 (ERC1) mRNA in the BC tissues and cells were detected by qRT-PCR. CCK8, colony formation, Transwell, and flow cytometry assays were performed to examine the cell proliferation, colony formation, cell invasion, and apoptosis, respectively, in the BC cells with regulated expressions of circ_0084927, miR-142-3p, and ERC1. RNase R treatment was employed to verify the circular structure of circ_0084927. Nucleocytoplasmic separation experiment, bioinformatics analysis, dual-luciferase reporter assay, and RNA immunoprecipitation were performed to investigate the ceRNA mechanism of circ_0084927. RESULTS: High levels of circ_0084927 and ERC1 and low levels of miR-142-3p were detected in the BC tissues and cells. Knockdown of circ_0084927 promoted apoptosis and inhibited proliferation, colony formation, and invasion of BC cells (all P<0.05), whereas overexpression of circ_0084927 in the BC cells achieved the opposite effects. miR-142-3p is the target of circ_0084927. Overexpression of miR-142-3p could inhibit BC cell proliferation, colony formation, and cell invasion and induce apoptosis of the BC cells (all P<0.05), and the effects of miR-142-3p knockout on the BC cells could be reversed by silencing circ_0084927. miR-142-3p could target ERC1. Both ERC1 silencing and circ_0084927 knockout in the BC cells could achieve the tumor-suppressing effect, and this effect could be more remarkable under simultaneous ERC1 silencing and circ_0084927 knockout (all P<0.05). CONCLUSION: Circ_0084927 can promote the progression of BC by regulating the miR-142-3p/ERC1 axis. AJTR
OBJECTIVE: We aimed to investigate the mechanism of circular RNA circ_0084927 in the progression of breast cancer (BC). METHODS: The levels of circ_0084927, miR-142-3p, and ELKS/RAB6-interacting/CAST family member-1 (ERC1) mRNA in the BC tissues and cells were detected by qRT-PCR. CCK8, colony formation, Transwell, and flow cytometry assays were performed to examine the cell proliferation, colony formation, cell invasion, and apoptosis, respectively, in the BC cells with regulated expressions of circ_0084927, miR-142-3p, and ERC1. RNase R treatment was employed to verify the circular structure of circ_0084927. Nucleocytoplasmic separation experiment, bioinformatics analysis, dual-luciferase reporter assay, and RNA immunoprecipitation were performed to investigate the ceRNA mechanism of circ_0084927. RESULTS: High levels of circ_0084927 and ERC1 and low levels of miR-142-3p were detected in the BC tissues and cells. Knockdown of circ_0084927 promoted apoptosis and inhibited proliferation, colony formation, and invasion of BC cells (all P<0.05), whereas overexpression of circ_0084927 in the BC cells achieved the opposite effects. miR-142-3p is the target of circ_0084927. Overexpression of miR-142-3p could inhibit BC cell proliferation, colony formation, and cell invasion and induce apoptosis of the BC cells (all P<0.05), and the effects of miR-142-3p knockout on the BC cells could be reversed by silencing circ_0084927. miR-142-3p could target ERC1. Both ERC1 silencing and circ_0084927 knockout in the BC cells could achieve the tumor-suppressing effect, and this effect could be more remarkable under simultaneous ERC1 silencing and circ_0084927 knockout (all P<0.05). CONCLUSION: Circ_0084927 can promote the progression of BC by regulating the miR-142-3p/ERC1 axis. AJTR