Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Mol Med Rep. 2021 Feb;23(2). doi: 10.3892/mmr.2020.11803. Epub 2020 Dec 23.
S100 calcium binding protein A16 (S100A16) is the most recent member of the S100 calcium-binding protein family. The function of S100A16 has been associated with various types of cancer; however, its role in colorectal cancer (CRC) remains unknown. Therefore, the aim of the present study was to investigate the role of S100A16 in CRC progression. The Oncomine dataset used in the current study revealed that the expression of S100A16 was decreased in CRC compared with normal colorectal tissues. Similar results were also determined via immunohistochemistry. In addition, a negative association was identified between S100A16 expression and the prognosis of patients with CRC. Further functional experiments revealed that S100A16 knockdown promoted the proliferation, migration and invasion of HCT116 and SW480 cells, and vice versa in Lovo cells. Epithelial-mesenchymal transition (EMT) was promoted and the JNK/p38 MAPK pathway was activated in HCT116 cells following S100A16 knockdown, as determined via western blotting. Furthermore, S100A16 silencing promoted the migration and invasion of cells. EMT was also reversed when cells were treated with the JNK inhibitor (SP600125) or the p38 inhibitor (SB203580). In summary, the results of the present study demonstrated that S100A16 suppressed the proliferation, migration and invasion of CRC cells partially via the JNK/p38 MAPK signalling pathway and subsequent EMT mediation.
S100 钙结合蛋白 A16（S100A16）是 S100 钙结合蛋白家族中最新的成员。S100A16 的功能与多种类型的癌症有关；然而，其在结直肠癌（CRC）中的作用尚不清楚。因此，本研究旨在探讨 S100A16 在 CRC 进展中的作用。本研究中使用的 Oncomine 数据集显示，与正常结直肠组织相比，CRC 中 S100A16 的表达降低。免疫组织化学也得出了类似的结果。此外，S100A16 表达与 CRC 患者的预后之间存在负相关。进一步的功能实验表明，S100A16 敲低促进了 HCT116 和 SW480 细胞的增殖、迁移和侵袭，而在 Lovo 细胞中则相反。Western blot 分析显示，S100A16 敲低促进了 HCT116 细胞中上皮-间充质转化（EMT）的发生，并激活了 JNK/p38 MAPK 通路。此外，S100A16 沉默促进了细胞的迁移和侵袭。当用 JNK 抑制剂（SP600125）或 p38 抑制剂（SB203580）处理细胞时，EMT 也被逆转。综上所述，本研究结果表明，S100A16 通过 JNK/p38 MAPK 信号通路和随后的 EMT 介导，部分抑制 CRC 细胞的增殖、迁移和侵袭。
