期刊
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
卷 126, 期 -, 页码 994-1001出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ijbiomac.2018.12.176
关键词
Cervical cancer; Radio sensitivity; GAS5; MiR-106b; IER3
资金
- National Natural Science Foundation of China [U1604172]
- Science and Technology Colleges Innovation Team Support Program of Henan Province [18IRTSTHN024]
- Science and Technology Planning Project of Henan Province [201701002]
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. (C) 2018 Elsevier B.V. All rights reserved.
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