Effect of picroside Ⅱ on the malignant progression of non-small cell lung cancer
- VernacularTitle:胡黄连苷Ⅱ对非小细胞肺癌恶性进展的影响
- Author:
Huanyu GUO
1
;
Weifang WANG
2
;
Liwei XU
3
;
Wenbo DONG
4
Author Information
1. Experimental Center，School of Clinical Medicine，Changchun University of Chinese Medicine，Changchun 130117，China
2. Dept. of Biochemistry，School of Clinical Medicine，Changchun University of Chinese Medicine，Changchun 130117，China
3. Dept. of Hematology and Oncology，the Affiliated Hospital of Changchun University of Chinese Medicine，Changchun 130112，China
4. Dept. of Clinical Laboratory，the Second Division of the First Hospital of Jilin University，Changchun 130061，China
- Publication Type:Journal Article
- Keywords:
picroside Ⅱ;
non-small cell lung cancer;
proliferation;
migration;
invasion;
sphingosine kinase 1/sphingosine-1-
- From:
China Pharmacy
2024;35(4):430-435
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the effect and mechanism of picroside Ⅱ on the malignant progression of non-small cell lung cancer （NSCLC）. METHODS A549 cells were divided into the control group， picroside Ⅱ low-， medium- and high- concentration groups， K6PC-5 [sphingosine kinase 1 （SPHK1） activator] group， and picroside Ⅱ high-dose+K6PC-5 group. Cell proliferation， migration and invasion were detected. Besides， the expression of proliferating cell nuclear antigen （PCNA）， matrix metalloproteinase-2 （MMP-2）， MMP-9， SPHK1， sphingosine-1-phosphate receptor 3 （S1PR3） and extracellular signal-regulated kinase 1/2 （ERK1/2） protein in the cells were also observed. BALB/c nude mice were subcutaneously inoculated with A549 cell suspension to establish NSCLC xenograft models. Then they were assigned to the nude mouse-control group， nude mouse-picroside Ⅱ low-， medium- and high-dose groups， nude mouse-K6PC-5 group， and nude mouse-picroside Ⅱ high-dose+K6PC-5 group （with 5 mice in each group） to investigate the effect of picroside Ⅱ on their tumor mass and volume. RESULTS Compared with the control group， the OD450 values， EdU-positive cell rates， scratch healing rates， cell invasion number， and the relative expression levels of PCNA， MMP-2， MMP-9， SPHK1， S1PR3 and ERK1/2 protein in the low-， medium- and high-concentration groups of picroside Ⅱ were significantly decreased. Compared with the nude mouse-control group， the tumor mass and volume in the nude mouse-low-， medium- and high-dose groups of picroside Ⅱ were significantly decreased or shrunk. The changes of above indicators were concentration/dose-dependent （P＜0.05）. The changing trend of the corresponding indicators in the K6PC-5 ZYTS181） group and the nude mouse-K6PC-5 group was opposite （P＜0.05）. Compared with the picroside Ⅱ high-concentration group or the nude mice-picroside Ⅱ high-dose group， the above quantitative indicators in the picroside Ⅱ high- concentration+K6PC-5 group cells and the nude mouse-picroside Ⅱ high-dose+K6PC-5 group nude mice were significantly increased or enlarged （P＜0.05）. CONCLUSIONS Picroside Ⅱ may inhibit the malignant progression of NSCLC by inhibiting SPHK1/sphingosine-1-phosphate/S1PR3 signaling pathway.
