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Different fate of cancer cells on several chemical functional groups

Self-assembled monolayers with different terminal chemical groups including thiol (SH), methyl (CH3), carboxyl (COOH) and hydroxyl (OH) were employed as substrates for the culture of hepatoma cells (HepG2s). X-ray photoelectron spectroscopy and atomic force microscopy confirmed the similar density o...

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Published in:Surface & coatings technology 2013-08, Vol.228, p.S48-S54
Main Authors: Yu, Xiao-Long, Xu, Su-Ju, Shao, Jun-Dong, Du, Chang, Chen, Shuang-Feng, Zhang, Bin, Wang, Yu-Xi, Wang, Xiu-Mei
Format: Article
Language:English
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Summary:Self-assembled monolayers with different terminal chemical groups including thiol (SH), methyl (CH3), carboxyl (COOH) and hydroxyl (OH) were employed as substrates for the culture of hepatoma cells (HepG2s). X-ray photoelectron spectroscopy and atomic force microscopy confirmed the similar density of different functional groups occupation. The adhesion and proliferation of cancer cells exhibited significant difference on different surfaces. The HepG2s adhered to CH3 surfaces but exhibited the smallest contact area with mostly rounded morphology, while those on SH surfaces exhibited the largest contact area with extensive spreading. The proliferation of HepG2s in prolonged culture was significantly inhibited on CH3 surface. Cells on other surfaces of various chemical groups proliferated at different levels. After 7days of culture, the proliferation of HepG2s on the different surfaces followed the trend: OH≈COOH>SH≫CH3. Due to the strong hydrophobic property, the CH3 group inhibited the cell adhesion, which led to the death of cancer cells. Compared with other chemical functional groups, the CH3 group exhibited its unique effect on the fate of cancer cells, providing a potential way on prevention and treatment of liver cancer. ► The effects of chemical groups on cancer cell were studied through SAM technique. ► The proliferation of HepG2s on the surfaces had the trend COOH~OH>SH≫CH3. ► The CH3 chemical group significantly inhibited the reproduction of HepG2s.
ISSN:0257-8972
1879-3347
DOI:10.1016/j.surfcoat.2012.08.054