Title:Tectorigenin Inhibits Glycolysis-induced Cell Growth and Proliferation by
Modulating LncRNA CCAT2/miR-145 Pathway in Colorectal Cancer
Volume: 24
Issue: 10
Author(s): Ying Xing, Bofan Lin, Baoxinzi Liu, Jie Shao and Zhichao Jin*
Affiliation:
- Department of Oncology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China
- Jiangsu
Province Hospital of Chinese Medicine, Nanjing, China
Keywords:
Tectorigenin, glycolysis, colorectal cancer, lncRNA CCAT2, microRNA-145, cell counting kit-8 (CCK-8).
Abstract:
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 realtime
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.
