Department of Oncology, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu, PR China.
Department of Pathology, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu, PR China.
Pathol Res Pract. 2020 Apr;216(4):152884. doi: 10.1016/j.prp.2020.152884. Epub 2020 Feb 13.
Colorectal cancer (CRC) is one of the most common diseases, accounting for about 10 % cancer-related deaths. Previous studies have found that caner-associated fibroblasts (CAFs) are closely related to the occurrence and metastasis of CRC, but the detailed mechanism is not precise.
Tumor cells and fibroblasts were co-cultured with a transwell system. Cell Counting Kit-8 and colony formation assays were performed to test the ability of cell proliferation. The flow cytometry was used to detect cell apoptosis. Western Blot was performed to assess protein expression levels. Quantitative real-time PCR was performed to detect mRNA expression levels. ERK5-IN-1 was used to inhibit the autophosphorylation of ERK5.
CAFs promoted cell proliferation and inhibited cell apoptosis in CRC cells. CAFs promoted the phosphorylation of ERK5 and the expression of programmed death-ligand 1 (PD-L1). Activated ERK5 promotes cell proliferation and inhibited cell apoptosis in CRC cells. The expression levels of ERK5 correlated with the expression of PD-L1 in CRC cells. CAFs promote cell growth by activating the ERK5/PD-L1 signaling axis in colorectal cancer.
CAFs significantly promoted cell proliferation and inhibited cell apoptosis in CRC cells, which features are dependent on regulating the ERK5/PD-L1 signaling axis.
结直肠癌（CRC）是最常见的疾病之一，约占癌症相关死亡人数的 10%。先前的研究发现，癌症相关成纤维细胞（CAFs）与 CRC 的发生和转移密切相关，但详细机制尚不清楚。
使用 Transwell 系统共培养肿瘤细胞和成纤维细胞。通过细胞计数试剂盒-8 和集落形成实验来测试细胞增殖能力。通过流式细胞术检测细胞凋亡。通过 Western Blot 评估蛋白表达水平。通过定量实时 PCR 检测 mRNA 表达水平。使用 ERK5-IN-1 抑制 ERK5 的自动磷酸化。
CAFs 促进 CRC 细胞的增殖并抑制细胞凋亡。CAFs 促进 ERK5 的磷酸化和程序性死亡配体 1（PD-L1）的表达。激活的 ERK5 促进 CRC 细胞的增殖并抑制细胞凋亡。ERK5 的表达水平与 CRC 细胞中 PD-L1 的表达水平相关。CAFs 通过激活 ERK5/PD-L1 信号通路促进结直肠癌细胞的生长。
CAFs 显著促进 CRC 细胞的增殖并抑制细胞凋亡，其特征依赖于调节 ERK5/PD-L1 信号通路。
