Yan Liu1, Huanhuan Li2, Yao Liu3, Zhichao Zhu4. 1. Department of Ophthalmology, Third Affiliated Hospital of Soochow University, China. Electronic address: onlyjsly@163.com. 2. Department of Ophthalmology, Third Affiliated Hospital of Soochow University, China. Electronic address: huanhuanli1008@163.com. 3. Department of Ophthalmology, Third Affiliated Hospital of Soochow University, China. 4. Department of Stomatology, Third Affiliated Hospital of Soochow University, China.
Abstract
OBJECTIVE: This study sought to explore the role of alpha-Enolase 1 (ENO1) in retinoblastoma (RB) which remains uncertain. METHODS: The expression of ENO1 in RB cell lines was examined by RT-qPCR and western blot. The biological function of ENO1 on cell proliferation in RB was determined in vitro. The predicted target of ENO1 was validated by dual-luciferase reporter assay and rescue experiment. The validation of clinical tissue samples was performed by RT-qPCR. RESULTS: Elevated ENO1 could promote the proliferation of RB cells. The dual luciferase reporter assay confirmed that ENO1 is the target for miR-22-3p. In rescue experiment, the result also indicated that miR-22-3p inhibits the proliferation of RB cells by negatively regulating the expression of ENO1. These differences were statistically significant (P<0.05). CONCLUSION: ENO1 functions as an oncogene in RB and inhibiting ENO1 by miR-22-3p suppresses the proliferation of RB cell lines. miR-22-3p/ENO1 pathway may serve as a novel target in RB.
OBJECTIVE: This study sought to explore the role of alpha-Enolase 1 (ENO1) in retinoblastoma (RB) which remains uncertain. METHODS: The expression of ENO1 in RB cell lines was examined by RT-qPCR and western blot. The biological function of ENO1 on cell proliferation in RB was determined in vitro. The predicted target of ENO1 was validated by dual-luciferase reporter assay and rescue experiment. The validation of clinical tissue samples was performed by RT-qPCR. RESULTS: Elevated ENO1 could promote the proliferation of RB cells. The dual luciferase reporter assay confirmed that ENO1 is the target for miR-22-3p. In rescue experiment, the result also indicated that miR-22-3p inhibits the proliferation of RB cells by negatively regulating the expression of ENO1. These differences were statistically significant (P<0.05). CONCLUSION:ENO1 functions as an oncogene in RB and inhibiting ENO1 by miR-22-3p suppresses the proliferation of RB cell lines. miR-22-3p/ENO1 pathway may serve as a novel target in RB.