Autophagy is an important action mode for functionalized selenium nanoparticles to exhibit anti-colorectal cancer activity
| Autor: | Siu To Cheung, Lizhen He, Zumei Liu, Kar Him Luk, Tianfeng Chen, Keith Kwong Hon Wong, Guanning Huang |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Programmed cell death Cell cycle checkpoint Colorectal cancer Biomedical Engineering Golgi Apparatus Antineoplastic Agents Apoptosis 02 engineering and technology Pleurotus Endocytosis Selenium 03 medical and health sciences Downregulation and upregulation Cell Line Tumor Autophagy medicine Humans General Materials Science Chemistry 021001 nanoscience & nanotechnology medicine.disease 030104 developmental biology Cancer cell Cancer research Nanoparticles Colorectal Neoplasms Lysosomes 0210 nano-technology |
| Zdroj: | Biomaterials Science. 6:2508-2517 |
| ISSN: | 2047-4849 2047-4830 |
| DOI: | 10.1039/c8bm00670a |
| Popis: | Selenium nanoparticles (SeNPs) have attracted much interest as potential anticancer nanodrugs. Our previous studies also demonstrated that SeNPs could be developed as carriers of clinically used anticancer drugs to achieve synergistic efficacy. Here, we describe the synthesis of Pleurotus tuber-regium (PTR)-conjugated SeNPs (PTR-SeNPs) and their application in the treatment of colorectal cancer (CRC), which is one of the principal causes of cancer morbidity and mortality in the world. PTR-SeNPs were absorbed by cancer cells via clathrin-mediated endocytosis into lysosomes and caveolae-mediated endocytosis into the Golgi apparatus. Internalized PTR-SeNPs trigger intracellular dose- and time-dependent G2/M phase arrest and apoptosis. Moreover, as shown by using a pEGFP-LC3 plasmid transfection model, PTR-SeNPs activate autophagy to promote the death of cancer cells via upregulation of beclin 1-related signaling pathways. In summary, this study demonstrates the high efficacy of functionalized SeNPs for therapy of colorectal cancer and reveals the important role of autophagy in promoting apoptosis and cell cycle arrest to induce cell death. |
| Databáze: | OpenAIRE |
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