Ampelopsin-sodium induces apoptosis in human lung adenocarcinoma cell lines by promoting tubulin polymerization in vitro
| Autor: | Kaihong Zang, Baolai Zhang, Yong-Jie Wu, Lijuan Zhu, Shuhong Dong, Jianyun Luo |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Cancer Research Cell ampelopsin sodium 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Microtubule medicine anti-tumor Mitosis biology Chemistry Cell growth apoptosis Cell migration Articles Cell cycle Cell biology Ampelopsin tubulin polymerization 030104 developmental biology medicine.anatomical_structure Tubulin human lung adenocarcinoma cell lines Oncology 030220 oncology & carcinogenesis biology.protein |
| Zdroj: | Oncology Letters |
| ISSN: | 1792-1082 1792-1074 |
| Popis: | Previous studies have demonstrated that ampelopsin (AMP), a type of flavonoid isolated from the stems and leaves of Ampelopsis grossedentata, exhibits anti-cancer activity in various types of cancer. Conversion of AMP into its sodium salt (AMP-Na) conferred enhanced solubility and stability to it. The present study aimed to evaluate the anti-cancer activity of AMP-Na in human lung adenocarcinoma cell lines and to investigate its mechanisms of action. Cell proliferation and viability were assessed by MTT and colony formation assays, and cell migration was determined using a scratch wound healing assay. The cell cycle distribution, apoptosis rate and tubulin immunofluorescence intensity were analyzed using flow cytometry, the cell ultra-microstructure was examined using transmission electron microscopy and the accumulation of tubulin was determined using laser confocal microscopy. The results demonstrated that AMP-Na significantly inhibited the proliferation, clonogenicity and migration of human lung adenocarcinoma cells. Furthermore, AMP-Na induced SPC-A-1 cell apoptosis, and promoted tubulin polymerization. The results suggested that the underlying mechanisms of AMP-Na may involve targeting of microtubules and tubulin polymerization to subsequently disrupt mitosis and induce cell cycle arrest at the S-phase. |
| Databáze: | OpenAIRE |
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