<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Huang Q</submitter><funding>National Natural Science Foundation of China</funding><pagination>e9559</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7380274</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8</volume><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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).&lt;h4>Results&lt;/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.&lt;h4>Conclusion&lt;/h4>EP inhibits glioblastoma cells migration and invasion by blocking NF-κB and ERK-mediated EMT.</pubmed_abstract><journal>PeerJ</journal><pubmed_title>Ethyl pyruvate inhibits glioblastoma cells migration and invasion through modulation of NF-κB and ERK-mediated EMT.</pubmed_title><pmcid>PMC7380274</pmcid><funding_grant_id>81372183</funding_grant_id><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Fu Y</pubmed_authors><pubmed_authors>Huang Q</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Chen S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Ethyl pyruvate inhibits glioblastoma cells migration and invasion through modulation of NF-κB and ERK-mediated EMT.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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).&lt;h4>Results&lt;/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.&lt;h4>Conclusion&lt;/h4>EP inhibits glioblastoma cells migration and invasion by blocking NF-κB and ERK-mediated EMT.</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2025-04-05T15:19:16.47Z</modification><creation>2025-04-05T15:19:16.47Z</creation></dates><accession>S-EPMC7380274</accession><cross_references><pubmed>32742812</pubmed><doi>10.7717/peerj.9559</doi></cross_references></HashMap>