Downregulation of GPR160 inhibits the progression of glioma through suppressing epithelial to mesenchymal transition (EMT) biomarkers

Background Glioma is one of the most fatal types of malignant tumours, the cause of which is mostly unknown. Orphan GPCRs (GPRs) have been previously implicated in tumour growth and metastasis. Therefore, these GPRs could prove to be alternative and promising therapeutic targets for cancer treatment...

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Published in:Basic & clinical pharmacology & toxicology 2022-10, Vol.131 (4), p.241-250
Main Authors: Abbas, Azar, Jun, Peng, Yuan, Jiang Yuan, Sun, Li, Jiang, Jinwei, Yuan, Shengtao
Format: Article
Language:English
Subjects:
Apoptosis
Biomarkers
Cell viability
cells proliferation
epithelial to mesenchymal transition (EMT)
Flow cytometry
Gene expression
Glioma
GPR160
Mesenchyme
Metastases
Metastasis
Therapeutic applications
Therapeutic targets
Tumors
Wound healing
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Summary:Background Glioma is one of the most fatal types of malignant tumours, the cause of which is mostly unknown. Orphan GPCRs (GPRs) have been previously implicated in tumour growth and metastasis. Therefore, these GPRs could prove to be alternative and promising therapeutic targets for cancer treatment. Objective The role of GPR160 in glioma has not yet been assessed. This study aims to explore the association of GPR160 with glioma progression and investigate its role in epithelial‐to‐mesenchymal transition (EMT) and metastasis. Methods Changes in protein expression were assessed using western blot analysis and immunofluorescent staining assays, while mRNA expression changes were evaluated using qRT‐PCR. To detect the changes in progression and metastasis, MTT, EdU proliferation, wound healing, transwell migration, and flow cytometry assays were carried out in vitro. An epithelial to mesenchymal phenotypic analysis was performed to detect EMT. Results We demonstrated that knockdown of GPR160 inhibited proliferation, colony formation, and cell viability and promoted apoptosis. Pro‐apoptotic biomarkers were upregulated, while anti‐apoptotic biomarkers were downregulated. Cell lines with GPR160 knockdown (GPR160 KD) showed a slowed migration rate and decreased invasion ability. EMT mesenchymal biomarkers were downregulated in GPR160 KD cell lines, while epithelial biomarkers were upregulated. Conclusion This study provides evidence that GPR160 is a potential therapeutic target in glioma for the first time. These findings can be used to discover in detail the molecular mechanism and pathways through which GPR160 promotes glioma progression.
ISSN:1742-7835
1742-7843
DOI:10.1111/bcpt.13769