Inhibitory effect of chikusetsusaponin IVa on proliferation of triple negative breast cancer cells
10.16438/j.0513-4870.2022-1313
- VernacularTitle:竹节参皂苷IVa抑制三阴性乳腺癌细胞增殖的研究
- Author:
Chen LIANG
1
;
Ying ZHOU
2
;
Chang-chang FAN
1
;
Ding XU
2
;
Qi WU
2
;
Ruo-lan HUANG
2
;
Yao XU
1
;
Ying LUO
1
,
3
Author Information
1. Wuhan University of Science and Technology, College of Life Sciences and Health, Wuhan 430065, China
2. Hubei Minzu University, Hubei Provincial Key Laboratory of Occurrence and Intervention of Rheumatic Diseases, College of Biological and Food Engineering, Enshi 445000, China
3. Hubei Minzu University, Hubei Provincial Key Laboratory of Occurrence and Intervention of Rheumatic Diseases, College of Biological and Food Engineering, Enshi 445000, China
- Publication Type:Research Article
- Keywords:
chikusetsusaponin IVa;
triple negative breast cancer;
cell proliferation;
cell cycle;
PI3K/AKT signaling pathway
- From:
Acta Pharmaceutica Sinica
2023;58(9):2677-2684
- CountryChina
- Language:Chinese
-
Abstract:
Chikusetsusaponin IVa (CsIVa) is a natural active monomer of triterpene saponins in the Chinese herbal medicine of Panax japonicus, which has anti-inflammatory, anti-tumor and other effects. However, its function and mechanism in triple negative breast cancer (TNBC) remain unclear. This study investigated the inhibitory effect and mechanisms of CsIVa on the proliferation of triple negative breast cancer cell line MDA-MB-231. In this study, we found that CsIVa could significantly inhibit the proliferation of MDA-MB-231 cells and eliminate its potential toxic effect on normal breast cells (MCF-10A). The transcriptome sequencing results showed that the inhibition of proliferation of MDA-MB-231 cells by CsIVa was closely related to cell cycle and the pathway regulating cell cycle. Further studies confirmed that CsIVa blocked the cell cycle in G2/M phase by down-regulating the expression of cyclin dependent kinase 1 (CDK1), cyclin B1 and up-regulating the expression of cyclin dependent kinase inhibitor 1A (p21). Moreover, CsIVa can block cell cycle through inhibiting PI3K/AKT signal pathway. In conclusion, CsIVa regulates the expression of cell cycle related proteins (p21, CDK1, cyclin B1) via inhibiting the activity of PI3K/AKT signaling pathway, blocks TNBC cell cycle, and thus exerts its anti-tumor activity.
