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RRM2 promotes the progression of human glioblastoma
Author(s) -
Li Chao,
Zheng Jingfang,
Chen Si,
Huang Bin,
Li Guosheng,
Feng Zichao,
Wang Jiwei,
Xu Shujun
Publication year - 2018
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.26529
Subject(s) - apoptosis , u87 , flow cytometry , cell growth , cancer research , gene silencing , biology , cell migration , glioblastoma , cell culture , immunology , gene , genetics
Glioblastoma pathogenesis is related to multiple processes that affected by dozens of regulatory factors, but the potential underlying factors regulating glioblastoma progression remains unclear. The goal of this research was to determine how the ribonucleotide reductase M2 subunit ( RRM2 ) influenced proliferation, invasion, migration, and apoptosis of human glioblastoma cells. The level of proliferation of human glioblastoma cells was measured through CCK8, colony formation assay and immunofluorescence stains. Flow cytometry (FCM), wound healing, and transwell assays were conducted to detect cell apoptosis, migration, and invasion. Apoptotic level of cells and invasion‐related expression of protein were measured by Western blot. Xenograft tumor model was established to confirm effect of RRM2 on the proliferation of human glioblastoma cells in vivo. Silencing RRM2 inhibited proliferation, invasion, and migration of glioblastoma cells whereas enhanced apoptosis rate. Overexpressing RRM2 promoted proliferation, migration and invasion but suppressed apoptosis. In vivo, Overexpressing RRM2 accelerated the tumor growth in glioblastoma cells. The present study illustrated that RRM2 was overexpressed in human glioblastoma cells. RRM2 promoted proliferation, migration, and invasion but inhibited apoptosis of human glioblastoma cells.