The mechanism of parthenolide strengthen vorinostat on inhibiting the proliferation of A549 non-small cell lung cancer cells
10.16438/j.0513-4870.2020-1034
- VernacularTitle:小白菊内酯增强伏立诺他抑制非小细胞肺癌A549细胞增殖的机制
- Author:
Yu-qing WANG
1
;
Meng-ying JI
1
;
Qiao-ru GUO
1
;
Rong WEI
1
;
Yue GAO
1
;
Yi-wen TAO
1
;
Jian-ye ZHANG
1
Author Information
1. Guangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou 511436, China
- Publication Type:Research Article
- Keywords:
parthenolide;
vorinostat;
synergistic effect;
non-small cell lung cancer;
mechanism
- From:
Acta Pharmaceutica Sinica
2020;55(9):2151-2156
- CountryChina
- Language:Chinese
-
Abstract:
This research explored the synergistic effects and the mechanism of parthenolide (PTL) and vorinostat (suberoylanilide hydroxamic acid, SAHA) on the proliferation of A549 non-small cell lung cancer cells. The combination effect of PTL and SAHA was detected by cell counting kit-8 (CCK-8) and colony formation assays. Scratch test was performed to detect cell migration. Annexin V-fluorescein isothiocyanate isomer/propidium iodide (FITC/PI) flow cytometry and Western blot analyses were used to determine cell apoptosis and its mechanism. The results showed that combination of PTL and SAHA inhibited the proliferation and migration of A549 with a synergistic effect compared to the single-drug groups. The combination of PTL and SAHA had synergistic effect to induce cell apoptosis by regulating p53 and c-myc pathways, and affected the expression levels of poly ADP-ribose polymerase (PARP), cysteinyl aspartate specific proteinase (caspase)-9, and caspase-3. Taken together, this study shows that combination of PTL and SAHA has synergistic effect, induces cell apoptosis and inhibits A549 proliferation, which is likely to be a novel strategy for the treatment of non-small cell lung cancer.
