1. GPR12 inhibits migration and promotes apoptosis in esophageal cancer and hypopharyngeal cancer cells
- Author
-
Wenming Jia, Xinliang Pan, Shuai Chen, Heng Liu, Ye Qian, Xiao-jie Ma, Xiaoqi Yang, Dapeng Lei, Minfa Zhang, and Juan Wang
- Subjects
0301 basic medicine ,Pulmonary and Respiratory Medicine ,Esophageal Neoplasms ,Apoptosis ,Transfection ,medicine.disease_cause ,epithelial‐to‐mesenchymal transition ,GPR12 ,migration ,Receptors, G-Protein-Coupled ,Flow cytometry ,03 medical and health sciences ,0302 clinical medicine ,Cell Movement ,medicine ,Humans ,Epithelial–mesenchymal transition ,esophageal cancer ,RC254-282 ,Orphan receptor ,Hypopharyngeal Neoplasms ,medicine.diagnostic_test ,business.industry ,Cancer ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Cell migration ,Original Articles ,General Medicine ,medicine.disease ,Head and neck squamous-cell carcinoma ,030104 developmental biology ,Oncology ,030220 oncology & carcinogenesis ,Cancer research ,Original Article ,Carcinogenesis ,business - Abstract
Background G protein‐coupled receptor 12 (GPR12) is an orphan receptor with no confirmed endogenous ligands. It plays important roles in both physiological and pathological conditions such as neurogenesis and neural inflammation. However, it remains unclear whether GPR12 regulates carcinogenesis and progression in head and neck squamous cell carcinoma (HNSCC), such as esophageal cancer (EC) and hypopharyngeal cancer (HC). Methods The Cancer Genome Atlas (TCGA) database was applied to explore the expression of GPR12. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to detect the expression of GPR12 in cancer tissues. Wound healing and transwell assays were carried out to verify the effect of GPR12 on cell migration. Flow cytometric analysis and caspase‐Glo 3/7 assay were carried out to verify the influence of GPR12 on cell apoptosis. Western blotting was used to measure the expression of proteins related to migration and apoptosis. Result The qRT‐PCR analyses showed that the expression of GPR12 decreased in EC and HC than that in their paired adjacent normal tissues. Wound healing assay and transwell assay demonstrated that GPR12 inhibited tumor cell migration. Flow cytometry analysis and Caspase‐Glo 3/7 Assay suggested that GPR12 promoted apoptosis. The mechanism of GPR12 may function via modulating caspase‐7, E‐cadherin, and α‐catenin in EC and HC cells. Conclusion In conclusion, GPR12 induced apoptosis by activating caspase‐7 and inhibited migration through epithelial‐to‐mesenchymal transition (EMT) in EC and HC. Our findings demonstrated that GPR12 as a potential tumor suppressor mediated cell migration and apoptosis in EC and HC., GPR12 induced apoptosis by activating caspase‐7 and inhibited migration through epithelial‐to‐mesenchymal transition (EMT) in EC and HC. Our findings demonstrated that GPR12 as a potential tumor suppressor mediated cell migration and apoptosis in EC and HC
- Published
- 2021