Jiang Shan, Yan Jiqi, Chen Xingsheng, Xie Qingji, Lin Wei, Lin Ting, Li Qinyu
Department of Vascular Thyroid Surgery, Union Hospital Affiliated to Fujian Medical University, Fuzhou, China.
Department of General Surgery, Ruijin Hospital Affiliated of Shanghai Jiaotong University School of Medicine, Shanghai, China.
Arch Med Sci. 2020 Feb 11;18(1):164-170. doi: 10.5114/aoms.2020.92871. eCollection 2022.
Thyroid cancer is an important disease that threatens the health of humans. Ginsenoside Rh2 is known as an anticancer molecule; however, its function in thyroid cancer cells has not been reported. In the present study, we identified that Rh2 treatment of the thyroid cancer cell line K1 inhibited cell migration and proliferation.
We determined the Rh2 function in thyroid cancer cell lines. By RT-PCR, expression of miR-524-5p and related genes were determined. The cell phenotype including cell migration and proliferation were detected after serials treatment. The relevant protein level were checked by Western blot.
Interestingly, we observed that miR-524-5p, a type of miRNA, had lower expression in the thyroid cancer cell lines TPC-1, K1, and NPA than in the normal thyroid cell line Nthyri3-1. Additionally, Rh2 treatment induced miR-524-5p expression. Further examination using overexpression of miR-524-5p identified that the miR-524-5p mimic inhibited cell migration and proliferation of the K1 line. Similar to Rh2-treated cells, the miR-524-5p mimic-expressing cells had increased E-cadherin and reduced vimentin levels compared to the control cells. Next, we examined the relationship between Rh2 and miR-524-5p with respect to thyroid cell migration and proliferation. Treatment with Rh2 and miR-524-5p inhibitor suppressed Rh2 action on K1 thyroid cell migration and proliferation, and the rates were similar to those in control cells, suggesting that Rh2 might induce miR-524-5p expression to inhibit thyroid cancer cell migration and proliferation.
Our analyses identified Rh2 and miR-524-5p action on thyroid cancer cell migration and proliferation as well as the linkage between Rh2 and miR-524-5p in thyroid cancer cell development.
甲状腺癌是一种威胁人类健康的重要疾病。人参皂苷Rh2被认为是一种抗癌分子；然而，其在甲状腺癌细胞中的功能尚未见报道。在本研究中，我们发现用Rh2处理甲状腺癌细胞系K1可抑制细胞迁移和增殖。
我们测定了Rh2在甲状腺癌细胞系中的功能。通过逆转录聚合酶链反应（RT-PCR），检测了miR-524-5p及相关基因的表达。在一系列处理后，检测细胞迁移和增殖等细胞表型。通过蛋白质免疫印迹法检测相关蛋白水平。
有趣的是，我们观察到一种名为miR-524-5p的微小RNA（miRNA）在甲状腺癌细胞系TPC-1、K1和NPA中的表达低于正常甲状腺细胞系Nthyri3-1。此外，Rh2处理可诱导miR-524-5p表达。使用miR-524-5p过表达进行进一步检测发现，miR-524-5p模拟物可抑制K1细胞系的细胞迁移和增殖。与用Rh2处理的细胞相似，与对照细胞相比，表达miR-524-5p模拟物的细胞中E-钙黏蛋白增加，波形蛋白水平降低。接下来，我们研究了Rh2与miR-524-5p在甲状腺细胞迁移和增殖方面的关系。用Rh2和miR-524-5p抑制剂处理可抑制Rh2对K1甲状腺细胞迁移和增殖的作用，其抑制率与对照细胞相似，这表明Rh2可能通过诱导miR-524-5p表达来抑制甲状腺癌细胞的迁移和增殖。
我们的分析确定了Rh2和miR-524-5p对甲状腺癌细胞迁移和增殖的作用，以及它们在甲状腺癌细胞发育过程中的联系。
