Department of Gastrointestinal Surgery, The Second People's Hospital of Liaocheng, Linqing, China.
J Clin Lab Anal. 2020 Oct;34(10):e23449. doi: 10.1002/jcla.23449. Epub 2020 Jul 23.
To investigate whether hsa_circ_0000520 affects Herceptin resistance in gastric cancer by regulating the PI3K-AKT signaling.
The expression of hsa_circ_0000520 was detected by qRT-PCR in gastric cancer tissues and cell lines. A Herceptin-resistant gastric cancer cell was established. PcDNA and pcDNA-hsa_circ_0000520 were transfected into NCI-N87R cells and treated with Herceptin at a concentration of 10 μg/mL for 24 hours. MTT tested cell proliferation, and apoptosis was measured by flow cytometry. IGF-1 treatment was used to activate PI3K-Akt signaling. The expression levels of related proteins were detected.
The expression of hsa_circ_0000520 was reduced in gastric cancer tissues and cell lines, and hsa_circ_0000520 in NCI-N87R cells was significantly lower than that of NCI-N87 cells. Compared with the CON group, the cell viability of the Herceptin group was significantly reduced, the apoptosis rate was significantly increased, the level of Bax protein was significantly increased, and the levels of Bcl-2, p-PI3K, and p-Akt protein were significantly reduced. Compared with the Herceptin + pcDNA group, the cell viability of the Herceptin + hsa_circ_0000520 group was significantly reduced, the apoptosis rate was significantly increased, the level of Bax protein was significantly increased, and the levels of p-PI3K and p-Akt proteins were significantly reduced. After IGF-1 treatment, the cell viability was significantly increased, the apoptosis rate was significantly reduced, the level of Bax protein was significantly reduced, and the level of Bcl-2 protein was significantly increased.
Hsa_circ_0000520 overexpression may reverse the Herceptin resistance of gastric cancer cells by inhibiting the PI3K-Akt signaling pathway.
研究 hsa_circ_0000520 是否通过调节 PI3K-AKT 信号通路影响胃癌对赫赛汀的耐药性。
采用 qRT-PCR 检测胃癌组织和细胞系中 hsa_circ_0000520 的表达。建立赫赛汀耐药性胃癌细胞系。将 PcDNA 和 pcDNA-hsa_circ_0000520 转染至 NCI-N87R 细胞中，用浓度为 10μg/mL 的赫赛汀处理 24 小时。MTT 检测细胞增殖，流式细胞术检测细胞凋亡。用 IGF-1 处理激活 PI3K-Akt 信号通路，检测相关蛋白的表达水平。
hsa_circ_0000520 在胃癌组织和细胞系中表达降低，NCI-N87R 细胞中的 hsa_circ_0000520 明显低于 NCI-N87 细胞。与 CON 组相比，赫赛汀组细胞活力明显降低，凋亡率明显升高，Bax 蛋白水平明显升高，Bcl-2、p-PI3K 和 p-Akt 蛋白水平明显降低。与赫赛汀+pcDNA 组相比，赫赛汀+hsa_circ_0000520 组细胞活力明显降低，凋亡率明显升高，Bax 蛋白水平明显升高，p-PI3K 和 p-Akt 蛋白水平明显降低。IGF-1 处理后，细胞活力明显升高，凋亡率明显降低，Bax 蛋白水平明显降低，Bcl-2 蛋白水平明显升高。
hsa_circ_0000520 过表达可能通过抑制 PI3K-Akt 信号通路逆转胃癌细胞对赫赛汀的耐药性。
