title: Constitutively active Akt contributes to vincristine resistance in human retinoblastoma cells.
abstract: Akt mediates survival signals which preserve various cancer cells from apoptosis. Its correlation with chemoresistance of cancer cells has attracted much attention. But how Akt affects vincristine-induced cell death in retinoblastoma is unknown. Here we show that Akt activity is involved in vincristine-induced cytotoxicity in retinoblastoma SO-Rb50 cells. Inhibition of Akt can decrease the survival of both sensitive and vincristine-resistant SO-Rb50 cells and increase the sensitivity of both cell lines to vincristine by enhancing the cell apoptosis and increasing the cellular accumulation of the drug. Akt may be a target for reducing drug resistance that improves the treatment for retinoblastoma.
authors.affiliation: Beijing Institute of Ophthalmology, Beijing Tong Ren Eye Centre, Beijing Tong Ren Hospital, Capital Medical University, Beijing, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Zhang
authors.forename: Bin
authors.initials: B
authors.lastname: Li
authors.forename: Shu-wei
authors.initials: SW
authors.lastname: Bai
authors.forename: Hui-juan
authors.initials: HJ
authors.lastname: Wang
mesh_terms: D002453:Cell Cycle; D016923:Cell Death; D045744:Cell Line, Tumor; D019008:Drug Resistance, Neoplasm; D006801:Humans; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D019572:Retinal Neoplasms / Q000378:metabolism*; D012175:Retinoblastoma / Q000378:metabolism* / Q000473:pathology; D014750:Vincristine / Q000494:pharmacology*
chemical_list: D014750:Vincristine; D051057:Proto-Oncogene Proteins c-akt