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pmid:30940290

Inhibition of Proliferation by Knockdown of Transmembrane (TMEM) 168 in Glioblastoma Cells via Suppression of Wnt/β-Catenin Pathway.

Jie Xu · Zhongzhou Su · Qiuping Ding · Liang Shen · Xiaohu Nie · Xuyan Pan · Ai Yan · Renfu Yan · Yue Zhou · Liqin Li · Bin Lu

Oncology research · 2019 doi:10.3727/096504018X15478559215014

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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pmid:30940290
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title
Inhibition of Proliferation by Knockdown of Transmembrane (TMEM) 168 in Glioblastoma Cells via Suppression of Wnt/β-Catenin Pathway.
doi
10.3727/096504018X15478559215014
pmid
30940290
authors array · 11 items
[0]
Jie Xu
[1]
Zhongzhou Su
[2]
Qiuping Ding
[3]
Liang Shen
[4]
Xiaohu Nie
[5]
Xuyan Pan
[6]
Ai Yan
[7]
Renfu Yan
[8]
Yue Zhou
[9]
Liqin Li
[10]
Bin Lu
journal
Oncology research
year
2019
abstract
Human glioblastoma multiforme (GBM) accounts for the majority of human brain gliomas. Several TMEM proteins, such as TMEM 45A, TMEM 97, and TMEM 140, are implicated in human brain gliomas. However, the roles of TMEM168 in human GBM remain poorly understood. Herein we found that mRNA levels of TMEM168 were overexpressed in GBM patients (n = 85) when compared with healthy people (n = 10), which was also supported by data from The Cancer Genome Atlas (TCGA). Kaplan-Meier analysis of Gene Expression Omnibus dataset GSE16011 suggested that enhanced TMEM168 expression was associated with shorter survival time. To investigate whether and how TMEM168 functioned in the tumorigenesis of human GBM cells, two human GBM cell lines (U87 and U373) were used for study. Lithium chloride (LiCl), an activator for Wnt/β-catenin pathway, was used for the treatment. Our data suggested that siRNA-TMEM168 (siTMEM168) prevented viability of U87 and U373 cells, induced cell cycle arrest (G0/G1 phase) and promoted apoptosis, and the mechanisms involved in blocking Wnt/β-catenin pathway, as evidenced by reducing expression of β-catenin, C-myc, cyclin D1, and survivin. Furthermore, the inhibited effect of siTMEM168 on human GBM cell growth was significantly alleviated with additional LiCl treatment, substantiating the involvement of the Wnt/β-catenin pathway in this process. In summary, our data demonstrated that TMEM168 may represent a therapeutic target for the treatment of human GBM.
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Then overall survival analysis was evaluated for mRNA expression of TMEM168 using the Kaplan–Meier method.
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sections[3] "Bioinformatics Analysis" paragraph 2
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a total of 529 expression data of TMEM168 in GBM patients and 10 expression data of TMEM168 in healthy people were also downloaded in The Cancer Genome Atlas (TCGA; https://cancergenome.nih.gov/cancersselected/glioblastomamultiforme) to make further confirmation of the results.
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a total of 529 expression data of TMEM168 in GBM patients and 10 expression data of TMEM168 in healthy people were also downloaded in The Cancer Genome Atlas (TCGA; https://cancergenome.nih.gov/cancersselected/glioblastomamultiforme) to make further confirmation of the results.
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Intrinsic Gene Expression Profiles of Gliomas are a Better Predictor of Survival than Histology
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Inhibition of Proliferation by Knockdown of Transmembrane (TMEM) 168 in Glioblastoma
[1]
d for the treatment. Our data suggested that siRNA-TMEM168 (siTMEM168) prevented viability of U
[2]
re, Treatment, and siRNA-TMEM168 (siTMEM168) Transfection Human GBM cell lines (U87 and U373; ATCC, Ma
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ere designed as shown in Table 1. Cells were transfected with siRNAs (20 μmol/L) via Lipofectamine 20
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cell cycle arrest (G0/G1 phase) and promoted apoptosis, and the mechanisms involved in blocking Wnt
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y of TMEM168 gene was detected by RT-PCR and Western blot, with the best knockdown effect being seen i
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Complete file
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Several TMEM proteins, such as TMEM 45A, TMEM 97, and TMEM 140, are implicated in human brain gliomas. However, the roles of TMEM168 in human GBM remain poorly understood. Herein we found that mRNA levels of TMEM168 were overexpressed in GBM patients (n = 85) when compared with healthy people (n = 10), which was also supported by data from The Cancer Genome Atlas (TCGA). Kaplan-Meier analysis of Gene Expression Omnibus dataset GSE16011 suggested that enhanced TMEM168 expression was associated with shorter survival time. To investigate whether and how TMEM168 functioned in the tumorigenesis of human GBM cells, two human GBM cell lines (U87 and U373) were used for study. Lithium chloride (LiCl), an activator for Wnt/β-catenin pathway, was used for the treatment. Our data suggested that siRNA-TMEM168 (siTMEM168) prevented viability of U87 and U373 cells, induced cell cycle arrest (G0/G1 phase) and promoted apoptosis, and the mechanisms involved in blocking Wnt/β-catenin pathway, as evidenced by reducing expression of β-catenin, C-myc, cyclin D1, and survivin. Furthermore, the inhibited effect of siTMEM168 on human GBM cell growth was significantly alleviated with additional LiCl treatment, substantiating the involvement of the Wnt/β-catenin pathway in this process. 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