VDAC1 Mediated Anticancer Activity of Gallic Acid in Human Lung Adenocarcinoma A549 Cells
| Autor: | Aikebaier Maimaiti, Hureshitanmu Kuerban, Amier Aili, Xuejun Li |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Cancer Research Lung Neoplasms Cell Survival Cell Adenocarcinoma of Lung Antineoplastic Agents Structure-Activity Relationship 03 medical and health sciences Western blot Gallic Acid Tumor Cells Cultured medicine Humans Viability assay Protein kinase B Cell Proliferation Pharmacology A549 cell Dose-Response Relationship Drug Molecular Structure medicine.diagnostic_test Chemistry Voltage-Dependent Anion Channel 1 Transfection Molecular biology 030104 developmental biology medicine.anatomical_structure A549 Cells Apoptosis Molecular Medicine Drug Screening Assays Antitumor VDAC1 |
| Zdroj: | Anti-Cancer Agents in Medicinal Chemistry. 18:255-262 |
| ISSN: | 1871-5206 |
| DOI: | 10.2174/1871520617666170912115441 |
| Popis: | Aims: Gallic acid (GA) is generally distributed in a variety of plants and foods, and possesses cell growth-inhibiting activities in cancer cell lines. In the present study, the impact of GA on cell viability, apoptosis induction and possible molecular mechanisms in cultured A549 lung carcinoma cells was investigated. Methods: In vitro experiments showed that treating A549 cells with various concentrations of GA inhibited cell viability and induced apoptosis in a dose-dependent manner. In order to understand the mechanism by which GA inhibits cell viability, comparative proteomic analysis was applied. The changed proteins were identified by Western blot and siRNA methods. Results: Two-dimensional electrophoresis revealed changes that occurred to the cells when treated with or without GA. Four up-regulated protein spots were clearly identified as malate dehydrogenase (MDH), voltagedependent, anion-selective channel protein 1(VDAC1), calreticulin (CRT) and brain acid soluble protein 1(BASP1). VDAC1 in A549 cells was reconfirmed by western blot. Transfection with VDAC1 siRNA significantly increased cell viability after the treatment of GA. Further investigation showed that GA down regulated PI3K/Akt signaling pathways. These data strongly suggest that up-regulation of VDAC1 by GA may play an important role in GA-induced, inhibitory effects on A549 cell viability. |
| Databáze: | OpenAIRE |
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