Tectorigenin Inhibits Glycolysis-induced Cell Growth and Proliferation by Modulating LncRNA CCAT2/miR-145 Pathway in Colorectal Cancer

被引:1
作者
Xing, Ying [1 ]
Lin, Bofan [1 ,2 ]
Liu, Baoxinzi [1 ,2 ]
Shao, Jie [1 ,2 ]
Jin, Zhichao [1 ,2 ]
机构
[1] Nanjing Univ Chinese Med, Affiliated Hosp, Dept Oncol, 155 Hanzhong Rd, Nanjing 210029, Peoples R China
[2] Jiangsu Prov Hosp Chinese Med, Nanjing, Peoples R China
基金
中国国家自然科学基金;
关键词
Tectorigenin; glycolysis; colorectal cancer; lncRNA CCAT2; microRNA-145; cell counting kit-8 (CCK-8); MIGRATION;
D O I
10.2174/0115680096274757231219072003
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background Colorectal cancer (CRC) places a heavy burden on global health. Tectorigenin (Tec) is a type of flavonoid-based compound obtained from the Chinese medical herb Leopard Lily Rhizome. It was found to exhibit remarkable anti-tumor properties in previous studies. However, the effect and molecular mechanisms of Tec in colorectal cancer have not been reported.Objective The objective of this study was to explore the action of Tec in proliferation and glycolysis in CRC and the potential mechanism with regard to the long non-coding RNA (lncRNA) CCAT2/micro RNA-145(miR-145) pathway in vitro and in vivo.Methods The anti-tumor effect of Tec in CRC was examined in cell and animal studies, applying Cell Counting Kit-8 (CCK-8) assay as well as xenograft model experiments. Assay kits were utilized to detect glucose consumption and lactate production in the supernatant of cells and animal serum. The expression of the glycolysis-related proteins was assessed by Western Blotting, and levels of lncRNA CCAT2 and miR-145 in CRC tissue specimens and cells were assessed by real-time quantitative PCR (RT-qPCR).Results Tec significantly suppressed cell glycolysis and proliferative rate in CRC cells. It could decrease lncRNA CCAT2 in CRC cells but increase the expression of miR-145. LncRNA CCAT2 overexpression or inhibition of miR-145 could abolish the inhibitive effects of Tec on the proliferation and glycolysis of CRC cells. The miR-145 mimic rescued the increased cell viability and glycolysis levels caused by lncRNA CCAT2 overexpression. Tec significantly inhibited the growth and glycolysis of CRC xenograft tumor. The expression of lncRNA CCAT2 decreased while the expression of miR-145 increased after Tec treatment in vivo.Conclusion Tec can inhibit the proliferation and glycolysis of CRC cells through the lncRNA CCAT2/miR-145 axis. Altogether, the potential targets discovered in this research are of great significance for CRC treatment and new drug development.
引用
收藏
页码:1071 / 1079
页数:9
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