Role of ENO1 in Glioblastoma Progression

Abstract

<p><strong><em>Objective</em></strong><strong>:</strong></p><p>To investigate whether and how ENO1 contributes to glioblastoma (GBM) progression.</p><p><strong><em>Method:</em></strong><br></p><p>In vitro studies were conducted using human GBM cell lines, U87 and U251. Knockdown of ENO1 and inhibition of ENO1 using an ENO1 inhibitor, ENOBlock, were done on the cell lines to examine the role of ENO1 in GBM. The effects of ENO1 knockdown and inhibition were evaluated by western blot, immunofluorescence staining, cell viability and proliferation assay, cell cycle analysis by flow cytometry, and colony formation.<br></p><p><strong><em>Result:</em></strong><br></p><p>Treatment with ENOBlock or knockdown of ENO1 decreases the cell viability and cell proliferation of GBM, but increases its cell death and sensitivity to temozolomide (TMZ). Treatment with ENOBlock also decreases mitochondrial membrane stability in GBM. Knockdown of ENO1 reduces colony formation of GBM and decreases the expression of mitochondrial proteins.<br></p><p><strong><em>Conclusion:</em></strong><br></p><p>ENO1 contributes to the progression of GBM and can potentially be a therapeutic target. Coadministration of TMZ and agents inhibiting the ENO1 signalling pathway can potentially produce synergistic therapeutic effects.<br></p>