Objective: The aim of the study was to investigate the biological role of growth arrest special 5 (GAS5) in the radio sensitivity of cervical cancer (CC).
Methods: The expressions of GAS5, miR-106b and immediate early response 3 (IER3) were detected in CC tissues and CC cell lines. RNA immunoprecipitation and RNA pull-down assays were performed to test the interaction of GAS5 and miR-106b. Dual-luciferase reporter assay was used to detect the regulatory relationship between miR-106b and IER3. The nude mouse model of CC was established for verifying the effects of GAS5 on the resistance of CC to radiation therapy in vivo.
Results: GAS5 and IER3 were low expressed in the radio-resistant human CC tissues and SiHa cells, while miR-106b expression was highly expressed. Overexpression of IER3 or GAS5 enhanced radio-sensitivity in SiHa cells, while knockdown of IER3 or GAS5 decreased radio-sensitivity in ME180 cells. Moreover, GAS5 served as a miR-106b sponge, and miR-106b negatively regulated IER3 expression. Besides, GAS5 could regulate IER3 expression through miR-106b, and GAS5 enhanced the radio-sensitivity in CC cells through inhibiting miR-106b both in vitro and in vivo.
Conclusion: Overexpression of GAS5 enhanced the sensitivity of CC cells to radiation treatment via up-regulating IER3 through miR-106b.
Keywords: Cervical cancer; GAS5; IER3; MiR-106b; Radio sensitivity.
Copyright © 2018 Elsevier B.V. All rights reserved.