[BAX Deletion Accelerates Progression of BCR-ABL-Induced B-ALL in Mice].
作者信息
Shi Liang, Long Yuan-Yuan, Sha Meng-QiSHA, Luo Xi, Huang Pei, Chen Yan
机构信息
Second Department of Pediatrics, Zunyi Medical University, Affiliated Hospital of Zunyi Medical University, The Children's Hospital of Guizhou Province, Zunyi 563003, Guizhou Province, China.
Second Department of Pediatrics, Zunyi Medical University, Affiliated Hospital of Zunyi Medical University, The Children's Hospital of Guizhou Province, Zunyi 563003, Guizhou Province, China,E-mail:
出版信息
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2020 Feb;28(1):29-33. doi: 10.19746/j.cnki.issn.1009-2137.2020.01.006.
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.
Zotero 插件