Yin Yanfen, Xu Wenwen, Song Yanan, Zhou Zhou, Sun Xin, Zhang Fengli
Department of Oncology, The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei 230031, Anhui, China.
The Graduate School, Anhui University of Traditional Chinese Medicine, Hefei 230038, Anhui, China.
Evid Based Complement Alternat Med. 2022 Jul 15;2022:1955101. doi: 10.1155/2022/1955101. eCollection 2022.
To clarify the mechanism of icariin (ICA) promoting gastric cancer (GC) cell apoptosis by regulating circ_0003159/eIF4A3/bcl-2 axis.
The mRNA or protein levels were detected by qRT-PCR or the western blot. The interaction between eIF4A3 protein and circ_0003159 or eIF4A3 protein and bcl-2 mRNA were validated by RNA pull down assays and the RNA immunoprecipitation (RIP) assay. The cell viability was measured by the cell counting kit (CCK)-8 kit. The cell apoptosis was measured by flow cytometry.
Compared with the group Vector, the ratio of cytoplasmic eIF4A3/nuclear eIF4A3 in the cell with circ_0003159 overexpression was significantly higher. RIP and RNA pull down results proved the interaction between eIF4A3 and circ_0003159. The RIP assay further validated the interaction between eIF4A3 and bcl-2. By gain or loss of the functional experiment, hsa_circ_0003159 was proved to recruit eIF4A3 to inhibit bcl-2 expression. Hsa_circ_0003159 regulates eIF4A3/bcl-2 to reduce GC cell viability and increase apoptosis Furthermore, ICA regulates hsa_circ_0003159/eIF4A3/bcl-2 axis to inhibit GC cell activity and induce GC cell apoptosis .
These data showed that ICA could effectively reduce the GC cell activity and induce GC cell apoptosis via hsa_circ_0003159/eIF4A3/bcl-2 axis, which provides new theoretical evidence for the treatment of GC by ICA.
阐明淫羊藿苷（ICA）通过调控circ_0003159/eIF4A3/bcl-2轴促进胃癌（GC）细胞凋亡的机制。
采用qRT-PCR或蛋白质免疫印迹法检测mRNA或蛋白质水平。通过RNA下拉试验和RNA免疫沉淀（RIP）试验验证eIF4A3蛋白与circ_0003159或eIF4A3蛋白与bcl-2 mRNA之间的相互作用。采用细胞计数试剂盒（CCK）-8试剂盒检测细胞活力。通过流式细胞术检测细胞凋亡。
与载体组相比，circ_0003159过表达细胞中细胞质eIF4A3/细胞核eIF4A3的比例显著更高。RIP和RNA下拉结果证明了eIF4A3与circ_0003159之间的相互作用。RIP试验进一步验证了eIF4A3与bcl-2之间的相互作用。通过功能实验的增减，证明hsa_circ_0003159招募eIF4A3抑制bcl-2表达。Hsa_circ_0003159调节eIF4A3/bcl-2以降低GC细胞活力并增加凋亡。此外，ICA调节hsa_circ_0003159/eIF4A3/bcl-2轴以抑制GC细胞活性并诱导GC细胞凋亡。
这些数据表明，ICA可通过hsa_circ_0003159/eIF4A3/bcl-2轴有效降低GC细胞活性并诱导GC细胞凋亡，为ICA治疗GC提供了新的理论依据。
