Nuclear protein-1 (NUPR1), also named as p8 or Com1, has been since found overexpressed in several human malignant tumor cells, such as glioma. NUPR1 also regulates cell cycle progression, however, the role of NUPR1 in regulating glioma cell cycle remains poorly understood. Knockdown efficiency of U87 and U251 cells infected with the lentiviral vector was detected by quantitative real-time PCR and western blot in vitro and in vivo. Flow cytometry and western blot were used to explore a mechanism by which NUPR1 modulates cell cycle in U87 and U251 cells. Immunohistochemistry was applied to detect expression levels of P27, CDK2, and cyclin E in human glioma tissues with NUPR1 positive expression and tumorigenesis in nude mice. We confirmed that the downregulation of NUPR1 arrested the cell cycle in the G0/G1 phase in U87 and U251 cells in vitro. Furthermore, the expression level of P27 was increased, and CDK2 and cyclin E were decreased upon silencing NUPR1 expression in vitro and in vivo. In conclusion, the knockdown of NUPR1 induces cell cycle arrest in the G0/G1 phase in glioma cells via P27.Glioma, the most common and malignant primary brain tumors, is characterized by low cure rate and high relapse rate. Even considering individual treatments, the survival time is still poor [1]. To date, more and more biomarkers were found to be related to the occurrence, growth, invasion and prognosis of glioma, but not be closely and high specificity, such as isocitrate dehydrogenase (IDH), O6-methylguanine-DNA methyltransferase (MGMT) and 1P19q (codeletion) loss [2]. NUPR1 (p8 or Com1), detected in pancreatic acinar cells of rats caused by acute pancreatitis, is located on human chromosome 16p11.2 and its gene encode a protein with a theoretical molecular

Abstractβ-Elemene is commonly used as an anti-cancer agent in different types of cancers and its effects on glioblastoma have been studied through different pathways. However, its effect through ring finger protein 135 (RNF135, OMIM 611358) (RNF135), which is upregulated in glioblastomas, has not yet been explored. The current study is focused on the effects of β-elemene on human glioblastoma cell lines U251, U118, A172 and U87 through RNF13 5. A cell counting kit-8 assay and wound healing assay have been utilized to test the proliferation and migration of the cells. Western blot and quantitative real-time-polymerase chain reaction (qRT-PCR) were used to evaluate the level of expression of RNF135. A model of nude mice was used to explore progression of the tumor in vivo. It was observed that increasing treatment time or dose of β-elemene remarkably decreased viability of the cells. The cells that were treated with β-elemene had a much lower speed of moving toward the gap in comparison to untreated cell lines. β-Elemene-treated cells showed a much lower level of expression of RNF135 mRNA than control groups (p <0.05) and the levels of RNF135 protein were lower in the cells treated with β-elemene than in control groups (p <0.05). Moreover, tumor progression in subcutaneous xenograft nude mice was delayed with the injection of β-elemene. Altogether, our findings suggest that β-elemene inhibits proliferation, migration and tumorigenicity of human glioblastoma cells through suppressing RNF135.