Effects of L-asparaginase on proliferation, cell cycle and apoptosis of Burkitt lymphoma cell lines
10.3760/cma.j.issn.0253-2727.2021.11.008
- VernacularTitle:左旋门冬酰胺酶对伯基特淋巴瘤细胞株增殖、细胞周期及凋亡的影响
- Author:
Dongyun TU
1
;
Meng ZHANG
;
Wenjing YIN
;
Linyan XU
;
Wei SANG
;
Zhenyu LI
;
Kailin XU
Author Information
1. 徐州医科大学血液病研究所，徐州医科大学附属医院细胞研究和转化医学中心，徐州医科大学附属医院血液科，徐州 221000
- Keywords:
Burkitt lymphoma;
L-asparaginase;
Apoptosis
- From:
Chinese Journal of Hematology
2021;42(11):930-938
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of L-asparaginase on the proliferation, cell cycle, and apoptosis of Burkitt lymphoma cell lines and explore the molecular mechanism.Methods:The effect of L-asparaginase on the cell proliferation of Burkitt lymphoma cell lines was detected using the CCK-8 method. The apoptosis rate and cell cycle were detected using flow cytometry. The expression of related molecules in cell cycle, apoptosis, autophagy, and PI3K/Akt/mTOR signaling pathway was detected and analyzed using qPCR and Western blot assay.Results:L-asparaginase significantly inhibited the proliferation of Burkitt lymphoma cell lines and caused cell cycle arrest at G 0/G 1 phage. L-asparaginase induced cell apoptosis and autophagy in Burkitt lymphoma cell lines. Further results showed that L-asparaginase inhibited the expression of c-Myc and also inhibited the expression of p-PI3K, p-Akt-S473, p-mTOR, p-70S6K, and p-4E-BP1. Combining PI3K inhibitor LY294002 with L-asparaginase further induced apoptosis. Additionally, L-Asp inhibited STAT and ERK signaling pathways. Conclusion:L-asparaginase inhibited Burkitt lymphoma cell proliferation, arrested cell cycle, activated autophagy, and induced apoptosis by inhibiting the PI3K/Akt/mTOR signaling pathway.
