01 September 2019 : Animal Research
Med Sci Monit 2019; 25:6563-6573
BACKGROUND: The aim of this study was to examine the effects and mechanisms of tenacigenin B in lymphoma treatment by in vitro and in vivo experiment.
MATERIAL AND METHODS: Raji cells were treated by difference methods. Measuring the cell proliferation of difference groups was done by MTT assay; cell apoptosis and cell cycle of difference groups were evaluated by flow cytometer; relative mRNA expression was evaluated by real-time polymerase chain reaction (RT-PCR), and relative protein expressions were measured by western blot assay in an in vitro study. In an in vivo study, we used a nude mice model to explore the anti-tumor effects and mechanism of tenacigenin B. Cell apoptosis was measured by TUNEL assay; relative protein expressions were evaluated by immunohistochemistry assay, and relative mRNA expression was evaluated by RT-PCR. In addition, the blood components of difference groups were measured.
RESULTS: Compared with the Normal control group, the cell proliferation rate was significantly downregulated, with cell apoptosis significantly increasing with G1 phase in the Drug group and the si-Aurora-A group (P<0.05, respectively). The PTEN, PI3K, AKT, P53, and P21 mRNA and protein expressions of the Drug group, the si-Aurora-A group, and the si-Aurora-A+Drug group were significantly different (P<0.01, respectively), The tumor volume and weight of the Drug group, the si-Aurora-A group, and the si-Aurora-A+Drug group were significantly suppressed compared with the Normal group (P<0.01, respectively). The positive apoptosis cell number in the Drug group, the si-Aurora-A group, and si-Aurora-A+Drug group were increased compared with that of Normal group (P<0.01, respectively).
CONCLUSIONS: Tenacigenin B had anti-tumor effects on lymphoma via regulation of Aurora-A in vitro and in vivo.
Keywords: Adenolymphoma, Apoptosis Inducing Factor, Aurora Kinase A, Cerebral Revascularization, Cell Cycle, Gene Expression Regulation, Neoplastic, Lymphoma, Mice, Inbred BALB C, Neoplasm Proteins, RNA, Messenger, Steroids
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