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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 3708048, 10 pages
https://doi.org/10.1155/2017/3708048
Research Article

Cellular Homeostasis and Antioxidant Response in Epithelial HT29 Cells on Titania Nanotube Arrays Surface

1Advanced Medical and Dental Institute, Universiti Sains Malaysia, Bertam, 13200 Kepala Batas, Penang, Malaysia
2School of Materials and Mineral Resources Engineering, Universiti Sains Malaysia, Engineering Campus, Nibong Tebal, 14300 South Seberang Perai, Penang, Malaysia
3Materials Technology Group, Industrial Technology Division, Nuclear Malaysia Agency, Bangi, 43000 Kajang, Selangor, Malaysia
4School of Distance Education, Universiti Sains Malaysia, 11800 Penang, Malaysia

Correspondence should be addressed to Rabiatul Basria SMN Mydin; ym.msu@airsablutaibar and Srimala Sreekantan; ym.msu@alamirs

Received 9 October 2016; Revised 1 December 2016; Accepted 7 December 2016; Published 28 February 2017

Academic Editor: Kota V. Ramana

Copyright © 2017 Rabiatul Basria SMN Mydin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Cell growth and proliferative activities on titania nanotube arrays (TNA) have raised alerts on genotoxicity risk. Present toxicogenomic approach focused on epithelial HT29 cells with TNA surface. Fledgling cell-TNA interaction has triggered G0/G1 cell cycle arrests and initiates DNA damage surveillance checkpoint, which possibly indicated the cellular stress stimuli. A profound gene regulation was observed to be involved in cellular growth and survival signals such as p53 and AKT expressions. Interestingly, the activation of redox regulator pathways (antioxidant defense) was observed through the cascade interactions of GADD45, MYC, CHECK1, and ATR genes. These mechanisms furnish to protect DNA during cellular division from an oxidative challenge, set in motion with XRRC5 and RAD50 genes for DNA damage and repair activities. The cell fate decision on TNA-nanoenvironment has been reported to possibly regulate proliferative activities via expression of p27 and BCL2 tumor suppressor proteins, cogent with SKP2 and BCL2 oncogenic proteins suppression. Findings suggested that epithelial HT29 cells on the surface of TNA may have a positive regulation via cell-homeostasis mechanisms: a careful circadian orchestration between cell proliferation, survival, and death. This nanomolecular knowledge could be beneficial for advanced medical applications such as in nanomedicine and nanotherapeutics.