Mechanisms of cladribine-inducing apoptosis of multiple myeloma RPMI 8226 cells in vitro

This study was purposed to explore the mechanisms of cladribine (2-CdA)-inducing apoptosis of multiple mycloma RPMI 8226 cells. The MTT method was used to determine cell proliferation after being treated with 2-CdA. Apoptosis and cell cycle progression were examined by flow cytometry. Transmission e...

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Published inZhongguo shi yan xue ye xue za zhi Vol. 22; no. 6; p. 1644
Main Authors Zhou, Nai-Cen, Qi, Mei-Ying, Liu, Bao-Lan, Xu, Bo, Liu, Xin
Format Journal Article
LanguageChinese
Published China 01.12.2014
Subjects
Apoptosis - drug effects
Caspase 3
Cell Division
Cell Line, Tumor
Cell Proliferation
Cladribine - pharmacology
Humans
Multiple Myeloma - pathology
Proto-Oncogene Proteins c-bcl-2
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Summary:This study was purposed to explore the mechanisms of cladribine (2-CdA)-inducing apoptosis of multiple mycloma RPMI 8226 cells. The MTT method was used to determine cell proliferation after being treated with 2-CdA. Apoptosis and cell cycle progression were examined by flow cytometry. Transmission electron microscopy was used to observe ultrastructural changes of RPMI 8226 cells. RT-PCR and Western blot were used to analyze the mRNA and protein expression levels of BCL-2, MCL-2 and caspase-3 respectively. The results showed that the 2-CdA inhibited proliferation of RPMI 8226 cells in time and dose-dependent manner. Typical apoptotic morphological and ultrastructure changes could be observed by electron microscopy. Flow cytometry showed that 2-CdA induced myeloma cell apoptosis and arrested myeloma cells in the G2/M phase. The mRNA expression of BCL-2 and MCL-1 decreased but that of caspase-3 not apparently changed. Western blot results suggested that the change trend of BCL-2 MCL-1 and caspase-3 was the same
ISSN:1009-2137
DOI:10.7534/j.issn.1009-2137.2014.06.027