Polydopamine Nanoparticles Activate Apelin/Apelin Receptor Signaling and Smad3 to Inhibit Tumor Cells in Lung Cancer

Author:

Yu Wuxin1,Liu Yuxin1,Lan Xiangning2,Zhou Yanjuan3,Wang Qiang3

Affiliation:

1. Wujin Hospital Affiliated to Jiangsu University, Wujin Clinical College, Xuzhou Medical University, Changzhou, Jiangsu, 213000, China

2. Wujin Hospital Affiliated to Jiangsu University, Changzhou Medical Center, Nanjing Medical University, Changzhou, Jiangsu, 213000, China

3. Wujin Hospital Affiliated to Jiangsu University, Wujin Clinical College, Xuzhou Medical University, Xuzhou Medical University Cancer Institute, Changzhou Medical Center, Nanjing Medical University, Changzhou, Jiangsu, 213000, China

Abstract

Lung cancer incidence is increasing and different concentrations of polydopamine nanoparticles may exert different anticancer effects. Apelin/APJ plays a certain role in lung cancer. This study focuses on the mechanism of polydopamine nanoparticles in Apelin/APJ signaling pathway activation Smad3 on tumor cells in lung cancer rats. 40 rats were randomly assigned into blank group, model group, low-dose, medium-dose, and high-dose groups of polydopamine nanoparticles followed by analysis of tumor weight, Apelin, APJ, Smad3 gene expression, tumor cell viability, cell apoptosis, Apelin, APJ, and Smad3 level. Polydopamine nanoparticles were successfully prepared. The polydopamine nanoparticle groups significantly inhibited tumor weight, and the medium-dose group decreased the most. And the groups significantly inhibited the gene expression of Apelin and APJ, with more inhibition in medium-dose group, P < 0.05. The polydopamine nanoparticle groups significantly up-regulated Smad3, inhibited tumor cell viability, and promoted apoptosis with significant changes in medium-dose group. In addition, the groups inhibited the protein expression of Apelin and APJ, and up-regulated Smad3, with more increase of Smad3 in medium-dose group, P < 0.05. Polydopamine nanoparticles may block the combination of Apelin and APJ by inhibiting the activity of Apelin/APJ pathway, which leads to further activation of Smad3, therefore inhibiting proliferation and promoting apoptosis of lung cancer cells. This process is related to down-regulation of Apelin expression.

Publisher

American Scientific Publishers

Reference33 articles.

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