ArticleCancer gene therapy2022
TMEM158 promotes the proliferation and migration of glioma cells via STAT3 signaling in glioblastomas.
Article in Cancer gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- The perinecrotic niche of glioblastoma drives tumor-associated macrophage polarization and immunosuppression via podoplanin-mediated CLEC5A activation.The Journal of clinical investigation · 2026Article
- Histone variant H2A.J is an epigenetic regulator of metastasis in lung adenocarcinoma.Cell death & disease · 2026Article
- Stattic engineering M2 macrophage-derived exosomes mediate autophagy and immune reprogramming for secondary hyperparathyroidism.Journal of advanced research · 2026Article
- TMEM158 promotes ICC metastasis via inducing lactic acid mediated reduction of actin skeleton stiffness of ICC cells.Journal of advanced research · 2026Article
- Research progress on TMEM proteins in cancer progression and chemoresistance (Review).International journal of molecular medicine · 2025Review
- TMEM150A overexpression was associated with poor prognosis and cancer progression in glioma verified by comprehensive analysis and cell experiments.Scientific reports · 2025Article
- The emerging role of transmembrane proteins in tumorigenesis and therapy.Translational cancer research · 2025Review
- Multilevel plasticity and altered glycosylation drive aggressiveness in hypoxic and glucose-deprived bladder cancer cells.iScience · 2025Article
- A clinically relevant model and method to study necrosis as a driving force in glioma restructuring and progression.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- NCAPH serves as a prognostic factor and promotes the tumor progression in glioma through PI3K/AKT signaling pathway.Molecular and cellular biochemistry · 2025Article
- Interrogation of macrophage-related prognostic signatures reveals a potential immune-mediated therapy strategy by histone deacetylase inhibition in glioma.Frontiers in oncology · 2025Article
- PCSK5 downregulation promotes the inhibitory effect of andrographolide on glioblastoma through regulating STAT3.Molecular and cellular biochemistry · 2025Article
- FGFR3-TACC3 fusion gene promotes glioblastoma malignant progression through the activation of STAT3 signaling pathway.Frontiers in oncology · 2025Article
- RAB32 promotes glioma cell progression by activating the JAK/STAT3 signaling pathway.The Journal of international medical research · 2024Article
- CH25H Promotes Autophagy and Regulates the Malignant Progression of Laryngeal Squamous Cell Carcinoma Through the PI3K-AKT Pathway.Cancer medicine · 2024Article
- Early human fetal lung atlas reveals the temporal dynamics of epithelial cell plasticity.Nature communications · 2024Article
- TGF-β-activated circRYK drives glioblastoma progression by increasing VLDLR mRNA expression and stability in a ceRNA- and RBP-dependent manner.Journal of experimental & clinical cancer research : CR · 2024Article
- TSPAN6 reinforces the malignant progression of glioblastoma via interacting with CDK5RAP3 and regulating STAT3 signaling pathway.International journal of biological sciences · 2024Article
- Xihuang pill facilitates glioma cell pyroptosis via the POU4F1/STAT3 axis.Functional & integrative genomics · 2023Article
- Therapeutic potential of pentamidine for glioma-initiating cells and glioma cells through multimodal antitumor effects.Cancer science · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
23 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is the most common primary intracranial malignant tumor in adults and has high morbidity and high mortality. TMEM158 has been reported to promote the progression of solid tumors. However, its potential role in glioma is still unclear. Here, we found that TMEM158 expression in human glioma cells in the tumor core was significantly higher than that in noncancerous cells at the tumor edge using bioinformatics analysis. Cancer cells in patients with primary GBMs harbored significantly higher expression of TMEM158 than those in patients with WHO grade II or III gliomas. Interestingly, regardless of tumor grading, human glioma samples that were IDH1-wild-type (IDH1-WT) exhibited higher expression of TMEM158 than those with IDH1-mutant (IDH1-Mut). We also illustrated that TMEM158 mRNA expression was correlated with poor overall survival in glioma patients. Furthermore, we demonstrated that silencing TMEM158 inhibited the proliferation of glioma cells and that TMEM158 overexpression promoted the migration and invasion of glioma cells by stimulating the EMT process. We found that the underlying mechanism involves STAT3 activation mediating TMEM158-driven glioma progression. In vivo results further confirmed the inhibitory effect of the TMEM158 downregulation on glioma growth. Collectively, these findings further our understanding of the oncogenic function of TMEM158 in gliomas, which represents a potential therapeutic target, especially for GBMs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.