{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Huang Q"],"funding":["National Natural Science Foundation of China"],"pagination":["e9559"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7380274"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8"],"pubmed_abstract":["<h4>Background</h4>Glioblastoma is a grade IV glioma with the highest degree of malignancy and extremely high incidence. Because of the poor therapeutic effect of surgery and radiochemotherapy, glioblastoma has a high recurrence rate and lethality, and is one of the most challenging tumors in the field of oncology. Ethyl pyruvate (EP), a stable lipophilic pyruvic acid derivative, has anti-inflammatory, antioxidant, immunomodulatory and other cellular protective effects. It has been reported that EP has potent anti-tumor effects on many types of tumors, including pancreatic cancer, prostate cancer, liver cancer, gastric cancer. However, whether EP has anti-tumor effect on glioblastoma or not is still unclear.<h4>Methods</h4>Glioblastoma U87 and U251 cells were treated with different concentrations of EP for 24 h or 48 h. CCK8 assay and Colony-Formation assay were performed to test the viability and proliferation. Wound-healing assay and Transwell assay were carried out to measure cell invasion and migration. Western blot was not only used to detect the protein expression of epithelial-mesenchymal transition (EMT)-related molecules, but also to detect the expression and activation levels of NF-κB (p65) and Extracellular Signal Regulated Kinase (ERK).<h4>Results</h4>In glioblastoma U87 and U251 cells treated with EP, the viability, proliferation, migration, invasion abilities were inhibited in a dose-dependent manner. EP inhibited EMT and the activation of NF-κB (p65) and ERK. With NF-κB (p65) and ERK activated, EMT, migration and invasion of U87 and U251 cells were promoted. However the activation of NF-κB (p65) and ERK were decreased, EMT, migration and invasion abilities were inhibited in U87 and U251 cells treated with EP.<h4>Conclusion</h4>EP inhibits glioblastoma cells migration and invasion by blocking NF-κB and ERK-mediated EMT."],"journal":["PeerJ"],"pubmed_title":["Ethyl pyruvate inhibits glioblastoma cells migration and invasion through modulation of NF-κB and ERK-mediated EMT."],"pmcid":["PMC7380274"],"funding_grant_id":["81372183"],"pubmed_authors":["Zhang Z","Zhang Y","Fu Y","Huang Q","Zhang S","Chen S"],"additional_accession":[]},"is_claimable":false,"name":"Ethyl pyruvate inhibits glioblastoma cells migration and invasion through modulation of NF-κB and ERK-mediated EMT.","description":"<h4>Background</h4>Glioblastoma is a grade IV glioma with the highest degree of malignancy and extremely high incidence. Because of the poor therapeutic effect of surgery and radiochemotherapy, glioblastoma has a high recurrence rate and lethality, and is one of the most challenging tumors in the field of oncology. Ethyl pyruvate (EP), a stable lipophilic pyruvic acid derivative, has anti-inflammatory, antioxidant, immunomodulatory and other cellular protective effects. It has been reported that EP has potent anti-tumor effects on many types of tumors, including pancreatic cancer, prostate cancer, liver cancer, gastric cancer. However, whether EP has anti-tumor effect on glioblastoma or not is still unclear.<h4>Methods</h4>Glioblastoma U87 and U251 cells were treated with different concentrations of EP for 24 h or 48 h. CCK8 assay and Colony-Formation assay were performed to test the viability and proliferation. Wound-healing assay and Transwell assay were carried out to measure cell invasion and migration. Western blot was not only used to detect the protein expression of epithelial-mesenchymal transition (EMT)-related molecules, but also to detect the expression and activation levels of NF-κB (p65) and Extracellular Signal Regulated Kinase (ERK).<h4>Results</h4>In glioblastoma U87 and U251 cells treated with EP, the viability, proliferation, migration, invasion abilities were inhibited in a dose-dependent manner. EP inhibited EMT and the activation of NF-κB (p65) and ERK. With NF-κB (p65) and ERK activated, EMT, migration and invasion of U87 and U251 cells were promoted. However the activation of NF-κB (p65) and ERK were decreased, EMT, migration and invasion abilities were inhibited in U87 and U251 cells treated with EP.<h4>Conclusion</h4>EP inhibits glioblastoma cells migration and invasion by blocking NF-κB and ERK-mediated EMT.","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020","modification":"2025-04-05T15:19:16.47Z","creation":"2025-04-05T15:19:16.47Z"},"accession":"S-EPMC7380274","cross_references":{"pubmed":["32742812"],"doi":["10.7717/peerj.9559"]}}