Xiong Lingfan, Guo Wenhao, Yang Yong, Gao Danping, Wang Jun, Qu Yuanyuan, Zhang Ying
Department of Oncology, China Resources & WISCO General Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, 430080, Hubei, China.
Department of Oncology, China Resources & WISCO General Hospital, Wuhan, 430080, Hubei, China.
Mol Cell Biochem. 2021 Jul;476(7):2729-2738. doi: 10.1007/s11010-021-04081-w. Epub 2021 Mar 8.
Colon cancer is one of the most familiar malignancies worldwide, with high morbidity and high mortality. This study intended to explore the role and mechanism of tectoridin (TEC) in regulating the progression of colon cancer. First, colon cancer cell lines (HCT116 and SW480 cells) were treated with different doses of TEC (0-200 μM). Then, CCK8 and clone formation experiments were performed to detect cell proliferation. Flow cytometry and western blot were conducted to examine apoptosis. Subsequently, Transwell assay and wound-healing test was employed to determine the effect of TEC on colon cancer cell invasion and migration. Next, western blot was performed to monitor the PKC/p38 MAPK pathway activation. In addition, a tumor model was established in nude mice to explore the effect of TEC on tumor growth in vivo. TEC dose-dependently dampened the proliferation, migration and invasion of colon cancer cells and facilitated their apoptosis. In addition, TEC abated the tumor cell growth in vivo. Besides, TEC dose-dependently suppressed the expression of PKC and p38 MAPK. Moreover, inhibiting the PKC pathway almost cancel out the anti-tumor effects induced by TEC. TEC attenuates the colon cancer progression by inhibiting the PKC/p38 MAPK pathway.
结肠癌是全球最常见的恶性肿瘤之一，发病率和死亡率都很高。本研究旨在探讨鸢尾苷（TEC）在调控结肠癌进展中的作用及机制。首先，用不同剂量的TEC（0 - 200 μM）处理结肠癌细胞系（HCT116和SW480细胞）。然后，进行CCK8和克隆形成实验以检测细胞增殖。采用流式细胞术和蛋白质免疫印迹法检测细胞凋亡情况。随后，运用Transwell实验和伤口愈合试验来确定TEC对结肠癌细胞侵袭和迁移的影响。接着，通过蛋白质免疫印迹法监测PKC/p38 MAPK通路的激活情况。此外，在裸鼠中建立肿瘤模型，以探究TEC对体内肿瘤生长的影响。TEC呈剂量依赖性地抑制结肠癌细胞的增殖、迁移和侵袭，并促进其凋亡。此外，TEC还能抑制体内肿瘤细胞的生长。此外，TEC呈剂量依赖性地抑制PKC和p38 MAPK的表达。而且，抑制PKC通路几乎消除了TEC诱导的抗肿瘤作用。TEC通过抑制PKC/p38 MAPK通路来减弱结肠癌的进展。
