LncRNA GAS5 confers the radio sensitivity of cervical cancer cells via regulating miR-106b/IER3 axis.

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). 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. 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. Overexpression of GAS5 enhanced the sensitivity of CC cells to radiation treatment via up-regulating IER3 through miR-106b.