Aim:To investigate the effect of 7-hydroxystaurosporine(UCN-01),a selectiveprotein kinase C(PKC)inhibitor,on cell growth,migration,and invasion in inva-sive human glioblastoma U-87MG cells.Methods:PKC activity was determinedbased on the PKC-catalyzed transfer of the ~(32)p-phosphate group from[g-~(32)p]ATPinto a PKC-specific peptide substrate.Cell viability was measured by MTT assay.Cell invasion and migration were evaluated by a Boyden chamber assay andscratch wound assay,respectively.Protein expression was analyzed using West-ern blot assay.The formation of 3-dimensional cellular aggregates was examinedby a cell-cell aggregation assay.Results:UCN-01 treatment resulted in concen-tration-and time-dependent inhibition of U-87MG cell growth at higher doses(>100 nmol/L),and reduced cell invasion and migration capability at less cytotoxicdoses(<100 nmol/L).UCN-01 significantly repressed PKC activity.Consistentwith this result,UCN-01 blocked cell invasion stimulated by phorbel 12-myristate-13-acetate(PMA)and ethanol(EtOH),2 PKC activators.Enforced expression ofthe tumor suppressor genes BRCA1 and PTEN increased the anti-invasion poten-tial of UCN-01.Exposure to UCN-01 caused a dose-dependent increase in celladhesion molecule E-cadherin.The effect of UCN-01 on the formation of cell-cellaggregation was significantly reduced by the addition of an anti-E-cadherinantibody.Conclusion:UCN-01 inhibits the invasion and migration of humanglioma cells.Accordingly,UCN-01 can have potential clinical applications for thetreatment of human glioma metastasis. Aim: To investigate the effect of 7-hydroxystaurosporine (UCN-01), a selective protein kinase C (PKC) inhibitor, on cell growth, migration, and invasion in inva- sive human glioblastoma U-87MG cells. Methods: PKC activity was determined on the PKC-catalyzed transfer of the ~ (32) p-phosphate group from [g- ~ (32) p] ATPinto a PKC-specific peptide substrate. Cell viability was measured by MTT assay. Cell invasion and migration were evaluated by a Boyden chamber assay and scratch wound assay, respectively. Protein expression was analyzed using West-ern blot assay. The formation of 3-dimensional cellular aggregates was examined by a cell-cell aggregation assay. Results: UCN-01 treatment resulted in concen- tration-and time-dependent inhibition of U-87MG cell growth at higher doses (> 100 nmol / L), and reduced cell invasion and migration capability at less cytotoxic doses (<100 nmol / L) .UCN-01 significantly repressed PKC activity. , UCN-01 blocked cell invasion stimulated by phorbel 12-myristate- 13-acetate (PMA) and ethanol (EtOH), 2 PKC activators. Enforced expression of the tumor suppressor genes BRCA1 and PTEN increased the anti-invasion poten- tial of UCN- 01. Expose to UCN-01 caused a dose- dependent increase in celladhesion molecule E-cadherin. The effect of UCN-01 on the formation of cell-cellaggregation was significantly reduced by the addition of an anti-E-cadherin antibody. Conlusion: UCN-01 inhibits the invasion and migration of humanglioma cells. Accredistically, UCN -01 can have potential clinical applications for the treatment of human glioma metastasis.