Targeting mitochondria with Au-Ag@Polydopamine nanoparticles for papillary thyroid cancer therapy.

Clicks: 433
ID: 343
2019
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #8 of 36 articles by views in Biomaterials science

Most read Least read

Bar heights use a square-root scale.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
The incidence of papillary thyroid cancer has rapidly increased in the past decade because of the progress in modern diagnostic technology. Novel therapeutic strategies for papillary thyroid cancer (which has low malignancy) based on organelle-targeted nanomaterials are greatly welcome in order to avoid over-treatment by conventional surgery. Herein, we demonstrate the mitochondria-targeted and exocytosis inhibition strategy of polydopamine (PDA)-coated inorganic nanoparticles (NPs) for enhanced papillary thyroid cancer therapy. PDA-coated gold-silver alloy NPs (Au-Ag@PDA NPs) were employed as the model of composite NPs. TPC-1 cells were chosen as the model of human papillary thyroid cancer cells. To better understand the effect of composite NPs on papillary thyroid cancer cells, the intracellular fate and corresponding cellular responses of Au-Ag@PDA NPs in TPC-1 cells were studied. The results indicate that Au-Ag@PDA NPs are internalized through a caveolae-mediated and macropinocytosis pathway and they are difficult to excrete by the TPC-1 cells. Au-Ag@PDA NPs mainly accumulate in mitochondria, resulting in the mitochondrial dysfunction and the decreased expression of dihydroorotate dehydrogenase. This leads to up-regulation of the p53 levels and therefore the S-phase cell cycle arrest and cell proliferation inhibition. In addition, despite cancer cells being able to survive by an autophagy-mediated pathway to escape apoptosis or necrosis, targeting mitochondria by Au-Ag@PDA NPs enables the destructive thermal ablation of TPC-1 cells by combination with photothermal therapy.
Reference Key
wang2019targeting Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Wang, Wenjing;Liu, Jie;Feng, Wenjie;Du, Shulin;Ge, Rui;Li, Jing;Liu, Yi;Sun, Hongchen;Zhang, Daqi;Zhang, Hao;Yang, Bai;
Journal Biomaterials science
Year 2019
DOI
10.1039/c8bm01414k
URL
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.