Constitutively active Akt contributes to vincristine resistance in human retinoblastoma cells.
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.
Zhang
Hao
H
Beijing Institute of Ophthalmology, Beijing Tong Ren Eye Centre, Beijing Tong Ren Hospital, Capital Medical University, Beijing, China.
Li
Bin
B
Bai
Shu-wei
SW
Wang
Hui-juan
HJ
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*
D014750:Vincristine; D051057:Proto-Oncogene Proteins c-akt