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[BAX Deletion Accelerates Progression of BCR-ABL-Induced B-ALL in Mice]
Liang Shi1, Yuan-Yuan Long1, Meng-QiSHA Sha1
1Second Department of Pediatrics, Zunyi Medical University, Affiliated Hospital of Zunyi Medical University, The Children's Hospital of Guizhou Province, Zunyi 563003, Guizhou Province, China.
Objective:
To explore whether BAX plays a role in the development of Philadelphia chromosome-positive leukemia and related mechanisms.
Methods:
Target-gene knockout mice were used as bone marrow cell donors. Retrovirus over-expressing BCR-ABL were packaged. BCR-ABL-induced B-ALL mouse model was established through donor's B cells transfected by the retrovirus and the B cells over-expressing BCR-ABL were given to the receptor mice by tail vein injection. Western blot was used to detect the protein express and flow cytometry was used to analyze the B cell subpopulations in BAX-/- and WT mouse bone marrows. Kaplan-Meier analysis was used to estimate the survival of diseased mice.
Results:
BAX deletion caused faster development of BCR-ABL-induced leukemia in vitro and in vivo. BCR-ABL increased BCL-2 expression and enhanced BCL-2/BAX heterodimer formation.
Conclusion:
The BAX deletion can accelerate the disease progression of BCR-ABL induced B-ALL.
