Faculty Collaboration Database

Inhibition of Bcl-xL expression sensitizes T-cell acute lymphoblastic leukemia cells to chemotherapeutic drugs. Leuk Res 2002 Mar;26(3):311-6

Date

01/17/2002

Pubmed ID

11792421

DOI

10.1016/s0145-2126(01)00118-7

Scopus ID

2-s2.0-0036138556 (requires institutional sign-in at Scopus site)   30 Citations

Abstract

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 NM

Author

Bruce m. Camitta Professor in the Pediatrics department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Antineoplastic Agents
Apoptosis
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