Gypenosides LI down-regulates CPT1B through the pathway of lipid metabolism to inhibit the growth of colon cancer
10.3969/j.issn.1006-5725.2025.02.002
- VernacularTitle:绞股蓝皂苷LI通过代谢脂肪酸通路下调肉碱棕榈酰转移酶1B抑制结肠癌生长
- Author:
Wenyu ZHU
1
;
Hongwei ZHANG
;
Decai TANG
;
Fangyuan CHEN
;
Hua JIANG
;
Haiyan MIN
;
Jie DING
Author Information
1. 南京医科大学第三附属医院(常州市第二人民医院)肿瘤中心,江苏常州 213000
- Publication Type:Journal Article
- Keywords:
Gypenoside LI;
carnitine Palmitoyltransferase 1b (CPT1B);
colon cancer;
fatty acid metabolism;
drug target
- From:
The Journal of Practical Medicine
2025;41(2):162-169
- CountryChina
- Language:Chinese
-
Abstract:
Objective To elucidate the mechanism through which Gypenoside L inhibits the growth of colon cancer by modulating carnitine palmitoyltransferase 1B (CPT1B),a pivotal enzyme in the fatty acid metabolism pathway. Methods Through in vitro experiments,various concentrations of Gypenoside LI LI were applied to inter-vene in colon cancer RKO and SW620 cells. The effects of Gypenoside LI on these cells were comprehensively evalu-ated using the CCK-8 assay,wound healing assay,colony formation assay,and live-dead cell staining,focusing on its impact on cell proliferation,migration,and apoptosis. Additionally,a human colon cancer tissue microarray (TMA) was utilized in conjunction with multiplex fluorescence immunohistochemistry to analyze the expression of CPT1B in colon cancer and adjacent tissues. SW620 cells were transfected with siRNA,and the mRNA and protein expression levels of CPT1B post-transfection were assessed using quantitative real-time PCR (qPCR) and Western blotting. Furthermore,an in vivo nude mouse colon cancer model was established to investigate the inhibitory effect of Gypenoside LI LI on colon cancer growth. Results In vitro experiments demonstrated that Gypenoside LI LI effectively inhibited the proliferation and migration of RKO and SW620 cells in a concentration-and time-dependent manner. Additionally,multiple fluorescence immunohistochemistry analyses revealed that the expression level of CPT1B in colon cancer tissues was significantly higher than that in adjacent non-tumor tissues. Gypenoside LI LI promoted ROS accumulation by inhibiting CPT1B expression. In vivo experiments further confirmed that Gypenoside LI LI could inhibit tumor formation in nude mice and reduce CPT1B expression. Conclusions This study elucidates the mechanism by which Gypenoside LI inhibits the growth of colon cancer cells. Specifically,it downregulates CPT1B,leading to increased accumulation of reactive oxygen species (ROS),disruption of fatty acid oxidation metabolism,and ultimately inducing apoptosis in colon cancer cells. These findings offer valuable insights into colon cancer treatment,suggesting new therapeutic strategies and potential drug targets.
