Cellular Homeostasis and Antioxidant Response in Epithelial HT29 Cells on Titania Nanotube Arrays Surface.
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.
Advanced Medical and Dental Institute, Universiti Sains Malaysia, Bertam, 13200 Kepala Batas, Penang, Malaysia.
Rabiatul Basria
0000-0001-8971-8809
RB
Smn Mydin
School of Materials and Mineral Resources Engineering, Universiti Sains Malaysia, Engineering Campus, Nibong Tebal, 14300 South Seberang Perai, Penang, Malaysia.
Srimala
0000-0001-5125-8683
S
Sreekantan
Materials Technology Group, Industrial Technology Division, Nuclear Malaysia Agency, Bangi, 43000 Kajang, Selangor, Malaysia.
Roshasnorlyza
R
Hazan
School of Distance Education, Universiti Sains Malaysia, 11800 Penang, Malaysia.
Mustafa Fadzil
0000-0003-1506-8713
MF
Farid Wajidi
Advanced Medical and Dental Institute, Universiti Sains Malaysia, Bertam, 13200 Kepala Batas, Penang, Malaysia.
Ishak
I
Mat
D017766:Acid Anhydride Hydrolases; D000975:Antioxidants / Q000378:metabolism*; D000071877:Checkpoint Kinase 1 / Q000235:genetics / Q000378:metabolism; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects; D045643:DNA Repair Enzymes / Q000235:genetics / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D059585:G1 Phase Cell Cycle Checkpoints / Q000187:drug effects; D019073:HT29 Cells; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D008855:Microscopy, Electron, Scanning; D043942:Nanotubes / Q000737:chemistry* / Q000633:toxicity; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D013499:Surface Properties; D014025:Titanium / Q000737:chemistry*; D059467:Transcriptome / Q000187:drug effects; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D000097642:GADD45 Proteins
D017766:Acid Anhydride Hydrolases; D000975:Antioxidants; D000071877:Checkpoint Kinase 1; D050760:Cyclin-Dependent Kinase Inhibitor p27; D045643:DNA Repair Enzymes; D004268:DNA-Binding Proteins; D047908:Intracellular Signaling Peptides and Proteins; D051057:Proto-Oncogene Proteins c-akt; D019253:Proto-Oncogene Proteins c-bcl-2; D014025:Titanium; D016159:Tumor Suppressor Protein p53; D000097642:GADD45 Proteins; C495901:TP53 protein, human; C009495:titanium dioxide; C112158:RAD50 protein, human