Inhibition of Bcl-xL expression sensitizes T-cell acute lymphoblastic leukemia cells to chemotherapeutic drugs. Leuk Res 2002 Mar;26(3):311-6
Date
01/17/2002Pubmed ID
11792421DOI
10.1016/s0145-2126(01)00118-7Scopus ID
2-s2.0-0036138556 (requires institutional sign-in at Scopus site) 30 CitationsAbstract
We have examined the effects of antisense oligonucleotides to bcl-x on the survival and chemosensitivity of CEM cells, a T-acute lymphoblastic leukemia (T-ALL) cell line. Also, we have measured the levels of Bcl-2, Bcl-x, and Bax in 20 cases of T-ALL. By 18 h after the bcl-x antisense treatment, CEM cells showed over a 75% reduction in the levels of Bcl-xL protein and over 30% decreased viable cell counts compared with cells treated with the control oligonucleotide. The combination of bcl-x antisense plus either dexamethasone or doxorubicin showed either strong synergistic or additive killing of CEM cells, respectively. These findings indicate that bcl-x antisense has cytotoxic activity and increases chemotherapy-induced cell death in CEM cells, a model for T-ALL.
Author List
Broome HE, Yu AL, Diccianni M, Camitta BM, Monia BP, Dean NMMESH terms used to index this publication - Major topics in bold
Antineoplastic AgentsApoptosis
Cell Division
Cells, Cultured
Dexamethasone
Doxorubicin
Gene Expression Regulation, Neoplastic
Humans
Leukemia-Lymphoma, Adult T-Cell
Oligodeoxyribonucleotides, Antisense
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-bcl-2
Recurrence
Tumor Cells, Cultured
bcl-2-Associated X Protein
bcl-X Protein
