TMEM140 is associated with the prognosis of glioma by promoting cell viability and invasion

Abstract

BackgroundGliomas are the most common types of primary brain tumors in the adult central nervous system. TMEM140 is identified as an amplified gene in the human gastric cancer genome. However, the function of TMEM140 in gliomas has not been thoroughly elucidated. The aim of the current study was to determine the clinical significance of TMEM140 expression in patients with gliomas and its effect on tumor cell malignant phenotypes.MethodsImmunohistochemical analysis and real-time reverse transcription PCR were performed to detect the expression levels of TMEM140 in 70 glioma brain tissue samples. Next, the correlation between the TMEM140 expression levels and the clinical characteristics and outcomes of glioma patients was statistically analyzed. TMEM140 expression was inhibited in two glioma cell lines (i.e., U87 and U373) using a knockdown method with small interfering RNA. Cell Counting Kit-8 and Transwell assays were used to investigate TMEM140 function during cell proliferation, invasion, and migration, respectively. Using flow cytometry and Western blot analysis, we subsequently determined the cell cycle and apoptosis profile of the TMEM140-silenced cells.ResultsTMEM140 protein expression was significantly higher in gliomas than in normal brain tissues (p < 0.0001). TMEM140 overexpression was strongly correlated with tumor size, histologic grade, and overall survival time (P < 0.05). TMEM140 decreased cell viability in vitro and dramatically decreased tumor volume in vivo. This phenomenon might be caused by G1 phase cell cycle arrest and cell apoptosis. TMEM140 silencing could suppress the viability, migration, and invasion of glioma cells.ConclusionsOur results suggest that TMEM140 expression is a prognostic factor that might play an important role in the viability, migration, and invasion of glioma cells. This study highlights the importance of TMEM140 as a novel prognostic marker and as an attractive therapeutic target for gliomas.

MST1 suppresses viability and promotes apoptosis of glioma cells via upregulating SIRT6 expression

“…Many proteins or other molecules related to the inhibition of glioma cell proliferation have been identified in previous studies (Yang et al, 2014;Wang et al, 2014). For example, transmembrane protein 140 (TMEM140) (Li et al, 2015) or centroso-mal protein of 55 (CEP55) (Wang et al, 2016) have been proved to promote viability of glioma cells, and silencing of TMEM140 or CEP55 could suppress the viability, migration, and invasion of glioma cells. Moreover, over-expression of miR-136 played a tumor-suppressive role in inducting glioma cell apoptosis (Yang et al, 2012).…”

High expression of Bruton’s tyrosine kinase (BTK) is required for EGFR-induced NF-κB activation and predicts poor prognosis in human glioma

“…Glioma is the most common form of malignant brain cancer in humans. Glioblastoma multiforme (GBM) is the most common and lethal subtypes of glioma [ 1 , 2 ]. Despite aggressive treatment with surgery, radiation and chemotherapy, the median survival for patients with GBM is merely 12 to 15 months [ 3 , 4 ].…”

Upregulation and biological function of transmembrane protein 119 in osteosarcoma

“…8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18 However, little is known regarding the association between TMEMs and osteosarcoma. TMEM119, a member of the transmembrane protein family and also known as osteoblast induction factor (Obif), is O -glycosylated at its N-terminal region.…”