S100A8 和 S100A9 通过 PI3K/Akt 信号通路对鼻咽癌细胞增殖的影响。
Influences of S100A8 and S100A9 on Proliferation of Nasopharyngeal Carcinoma Cells through PI3K/Akt Signaling Pathway.
机构信息
Department of Otolaryngology-Head and Neck Surgery, Xijing Hospital, Air Force Medical University, China.
出版信息
Biomed Res Int. 2021 Sep 24;2021:9917365. doi: 10.1155/2021/9917365. eCollection 2021.
OBJECTIVE
To investigate the effects of S100A8 and S100A9 on proliferation in nasopharyngeal carcinoma cells and the regulatory effects of PI3K/Akt signaling pathway.
METHODS
Nasopharyngeal carcinoma cells (CNE1) were cultured and randomly divided into three groups: control group, S100A8/S100A9 overexpression group, and siRNA S100A8/S100A9 group. CCK-8 method was used to detect the effect of S100A8 and S100A9 on the viability of nasopharyngeal carcinoma cells. The effects of S100A8 and S100A9 on the colony forming ability of nasopharyngeal carcinoma cells were detected by colony forming assay. The effects of S100A8 and S100A9 on the proliferation of nasopharyngeal carcinoma cells were detected by EdU staining. The mRNA levels of PI3K and Akt were detected by RT-PCR. The expression levels of PI3K and Akt in NPC cells were detected by Western blot. Wortmannin, an inhibitor of PI3K/Akt pathway, was used to inhibit the activation of PI3K/Akt pathway.
RESULTS
Compared with the control group, the cell viability, the number of plate clones, the positive rate of EdU staining, and the mRNA and protein levels of PI3K and Akt were increased in the overexpression group. Compared with the control group, the cell viability, the number of plate clones, the positive rate of EdU staining, and the mRNA and protein levels of PI3K and Akt were decreased in the siRNA group. After inhibiting the activation of PI3K/Akt pathway, the viability of NPC cells in the overexpression group decreased significantly at 48 h and 72 h, while that in the siRNA group increased significantly.
CONCLUSION
SiRNA S100A8 and S100A9 could inhibit the proliferation of nasopharyngeal carcinoma cells, and the underlying mechanism may be related to the inhibition of PI3K/Akt signaling pathway.
目的
研究 S100A8 和 S100A9 对鼻咽癌细胞增殖的影响及 PI3K/Akt 信号通路的调节作用。
方法
培养鼻咽癌细胞（CNE1），并随机分为三组：对照组、S100A8/S100A9 过表达组和 siRNA S100A8/S100A9 组。CCK-8 法检测 S100A8 和 S100A9 对鼻咽癌细胞活力的影响。集落形成实验检测 S100A8 和 S100A9 对鼻咽癌细胞集落形成能力的影响。EdU 染色检测 S100A8 和 S100A9 对鼻咽癌细胞增殖的影响。RT-PCR 检测 PI3K 和 Akt 的 mRNA 水平。Western blot 检测 NPC 细胞中 PI3K 和 Akt 的表达水平。用 PI3K/Akt 通路抑制剂 wortmannin 抑制 PI3K/Akt 通路的激活。
结果
与对照组相比，过表达组细胞活力、平板克隆数、EdU 染色阳性率及 PI3K 和 Akt 的 mRNA 和蛋白水平均升高；与对照组相比，siRNA 组细胞活力、平板克隆数、EdU 染色阳性率及 PI3K 和 Akt 的 mRNA 和蛋白水平均降低。抑制 PI3K/Akt 通路激活后，过表达组 NPC 细胞活力在 48 h 和 72 h 时明显下降，而 siRNA 组明显升高。
结论
siRNA S100A8 和 S100A9 可抑制鼻咽癌细胞增殖，其作用机制可能与抑制 PI3K/Akt 信号通路有关。
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