Novel self-micellizing anticancer lipid nanoparticles induce cell death of colorectal cancer cells
- Authors
- Sundaramoorthy, Pasupathi; Baskaran, Rengarajan; Mishra, Siddhartha Kumar; Jeong, Keun-Yeong; Oh, Seung Hyun; Yoo, Bong Kyu; Kim, Hwan Mook
- Issue Date
- 1-Nov-2015
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- Nanoparticle; Self-micellizing anticancer lipid; Apoptosis; Autophagy; Colorectal cancer
- Citation
- COLLOIDS AND SURFACES B-BIOINTERFACES, v.135, pp.793 - 801
- Journal Title
- COLLOIDS AND SURFACES B-BIOINTERFACES
- Volume
- 135
- Start Page
- 793
- End Page
- 801
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/9948
- DOI
- 10.1016/j.colsurfb.2015.08.039
- ISSN
- 0927-7765
- Abstract
- In the present study, we developed a novel drug-like self-micellizing anticancer lipid (SMAL), and investigated its anticancer activity and effects on cell death pathways in human colorectal cancer (CRC) cell lines.-Three self-assembled nanoparticles were prepared, namely, SMAL102 (lauramide derivative), SMAL104 (palmitamide derivative), and SMAL108 (stearamide derivative) by a thin-film hydration technique, and were characterized for physicochemical and biological parameters. SMAL102 were nanosized (160.23 +/- 8.11 nm) with uniform spherical shape, while SMAL104 and SMAL108 did not form spherical shape but formed large size nanoparticles and irregular in shape. Importantly, SMAL102 showed a cytotoxic effect towards CRC cell lines (HCT116 and HT-29), and less toxicity to a normal colon fibroblast cell line (CCD-18Co). Conversely, SMAL104 and SMAL108 did not have an anti-proliferative effect on CRC cell lines. SMAL102 nanoparticles were actively taken up by CRC cell lines, localized in the cell membrane, and exhibited remarkable cytotoxicity in a concentration-dependent manner. The normal colon cell line showed significantly less cellular uptake and non-cytotoxicity as compared with the CRC cell lines. SMAL102 nanoparticles induced caspase-3, caspase-9, and PARP cleavage in HT-29 cells, indicating the induction of apoptosis; whereas LOB was activated in HCT116 cells, indicating autophagy-induced cell death. Collectively, these results demonstrate that SMAL102 induced cell death via activation of apoptosis and autophagy in CRC cell lines. The present study could be a pioneer for further preclinical and clinical development of such compounds. (c) 2015 Elsevier B.V. All rights reserved.
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