[Effects of Emodin Derivative on Cell Cycle, Apoptosis and NF-κB Pathway in Burkitt Lymphoma Cells].
Raji cell
Burkitt's lymphoma
MTT assay
BCL6
DOI:
10.19746/j.cnki.issn.1009-2137.2021.02.027
Publication Date:
2021-04-01
AUTHORS (9)
ABSTRACT
OBJECTIVE To investigate the effect and mechanism of a novel emodin derivative YX-18 on Burkitt lymphoma (BL) cells. METHODS MTT assay was used to detect proliferation BL cell lines CA46 Raji. Annexin V-PE/7-AAD double staining for detecting apoptosis Raji PI/RNase test cycle. JC-1 method measure changes mitochondrial membrane potential after treatment, DAPI morphology apoptotic Western blot analyze distribution NF-κB pathway protein (P65, P-P65, IκB, P-IκB) in cytoplasm nucleus, also expression cyclin-related P21, CDK2, P-CDK2, Cycling D1, E1, apoptosis-related Caspase-3, Caspase-8, Caspase-9 proliferation-related C-MYC, BCL-2 by YX-18. Real-time fluorescence-quantitative PCR evaluate effects mRNA levels C-MYC Ki-67 genes cells, EBNA-1 EBER EBV (EBV+) RESULTS Novel Emodin could effectively inhibit Raji, showing time-dependent (24, 48 72 h: rCA46=0.89, 0.75, rRaji=0.87, 0.73, 0.64). IC50 cells treated with 24 h 1.77±0.04 µmol/L 1.97±0.22µmol/L, respectively. were at concentration 2.0 4.0 h. Compared control group, both strains showed very significant (P<0.01), concentration-dependent (rCA46=0.99, rRaji=0.92). Moreover, cleavaged 8 9 proteins activated into verious degrees two lines. Both displayed cycle arrest G0/G1 phase (P<0.01) exposed hours 1.0, 0.5 1 decreased level cyclin p-cdk2 increased p21Waf1/Cip1 significantly declined µmol/l manner (rCA46=-0.96, rRaji=-0.99). tests indicated that down-regulated nucleus P65 intracellular P65, P-IκB, P-P65 protein, upregulated IκB dose-dependent manner. Meanwhile, molecules significantly. suppressed lines, EBV-positive way. CONCLUSION The can induce arrest. inhibitory may be related Caspase pathway, molecules, such as Ki-67, inhibition pathway.
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