Hongbin Wang1, Hua Zhi2, Dongzhou Ma1, Tao Li3. 1. Department of Neurosurgery, Affiliated Hospital of Hebei University of Engineering, Handan 056029, Hebei, China. 2. Department of Cardiovascular Medicine, Affiliated Hospital of Hebei University of Engineering, Handan 056029, Hebei, China. 3. Department of Neurosurgery, Affiliated Hospital of Hebei University of Engineering, Handan 056029, Hebei, China. Electronic address: aiminzhang2000@126.com.
Abstract
AIM: To study the effects of miR-217 on glioblastoma cell proliferation, migration and invasion and its regulation on YWHAG. METHODS: QRT-PCR was used to detect the expression of related mRNAs and miRNA in both glioblastoma tissues and cells. Western blot was used to determine the protein expression of related genes. The transfection was performed using lipo2000. MTT assay, colony formation assay, wound healing assay, Transwell assay as well as flow cytometry were employed to determine the viability, proliferation, migration, invasion and mitosis of UG87 MG cell line. Besides, the dual luciferase reporter gene assay was used to determine the direct targeting relationship between miR-217 and YWHAG. Xenograft models were also constructed and the effect of miR-217 on tumor growth was studied in vivo. RESULTS: MiR-217 was up-regulated, whereas YWHAG was down-regulated in glioblastoma tissues and cells. The down-regulation of miR-217 or the up-regulation of YWHAG suppressed the viability, proliferation, migration, invasion and mitosis of U87 MG cells in vitro. In addition, MiR-217 directly targeted 3'UTR of YWHAG and suppressed the expression of YWHAG. Up-regulation of miR-217 could efficiently attenuate the inhibitory effects of YWHAG overexpression on the proliferation and metastasis of U87 MG cells. YWHAG was able to accelerate the phosphorylation of MDM4 and lead to the degradation of P53, which provides a potential mechanism for the tumor-promoting role of miR-217 in glioblastoma cells. By constructing xenograft models, it was also confirmed that miR-217 could promote tumor growth in vivo. CONCLUSION: MiR-217 could promote the viability, proliferation, migration, invasion and mitosis of glioblastoma cells both in vitro and in vivo.
AIM: To study the effects of miR-217 on glioblastoma cell proliferation, migration and invasion and its regulation on YWHAG. METHODS: QRT-PCR was used to detect the expression of related mRNAs and miRNA in both glioblastoma tissues and cells. Western blot was used to determine the protein expression of related genes. The transfection was performed using lipo2000. MTT assay, colony formation assay, wound healing assay, Transwell assay as well as flow cytometry were employed to determine the viability, proliferation, migration, invasion and mitosis of UG87 MG cell line. Besides, the dual luciferase reporter gene assay was used to determine the direct targeting relationship between miR-217 and YWHAG. Xenograft models were also constructed and the effect of miR-217 on tumor growth was studied in vivo. RESULTS:MiR-217 was up-regulated, whereas YWHAG was down-regulated in glioblastoma tissues and cells. The down-regulation of miR-217 or the up-regulation of YWHAG suppressed the viability, proliferation, migration, invasion and mitosis of U87 MG cells in vitro. In addition, MiR-217 directly targeted 3'UTR of YWHAG and suppressed the expression of YWHAG. Up-regulation of miR-217 could efficiently attenuate the inhibitory effects of YWHAG overexpression on the proliferation and metastasis of U87 MG cells. YWHAG was able to accelerate the phosphorylation of MDM4 and lead to the degradation of P53, which provides a potential mechanism for the tumor-promoting role of miR-217 in glioblastoma cells. By constructing xenograft models, it was also confirmed that miR-217 could promote tumor growth in vivo. CONCLUSION:MiR-217 could promote the viability, proliferation, migration, invasion and mitosis of glioblastoma cells both in vitro and in vivo.
Authors: Francesca Megiorni; Moreno Colaiacovo; Samantha Cialfi; Heather P McDowell; Alessandro Guffanti; Simona Camero; Armando Felsani; Paul D Losty; Barry Pizer; Rajeev Shukla; Carlo Cappelli; Eva Ferrara; Antonio Pizzuti; Anna Moles; Carlo Dominici Journal: Oncol Rep Date: 2017-06-06 Impact factor: 3.906