Evidence map›Paper›PMID 28337249›Full record

ArticleOxidative medicine and cellular longevity2017

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

Rabiatul Basria Smn Mydin, Srimala Sreekantan, Roshasnorlyza Hazan, Mustafa Fadzil Farid Wajidi, Ishak Mat

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 52% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Rabiatul Basria Smn MydinAdvanced Medical and Dental Institute, Universiti Sains Malaysia, Bertam, 13200 Kepala Batas, Penang, Malaysia.ORCID 0000-0001-8971-8809
Srimala SreekantanSchool of Materials and Mineral Resources Engineering, Universiti Sains Malaysia, Engineering Campus, Nibong Tebal, 14300 South Seberang Perai, Penang, Malaysia.ORCID 0000-0001-5125-8683
Roshasnorlyza HazanMaterials Technology Group, Industrial Technology Division, Nuclear Malaysia Agency, Bangi, 43000 Kajang, Selangor, Malaysia.
Mustafa Fadzil Farid WajidiSchool of Distance Education, Universiti Sains Malaysia, 11800 Penang, Malaysia.ORCID 0000-0003-1506-8713
Ishak MatAdvanced Medical and Dental Institute, Universiti Sains Malaysia, Bertam, 13200 Kepala Batas, Penang, Malaysia.
Universiti Sains Malaysia · MYMalaysian Nuclear Agency · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Acid Anhydride HydrolasesAntioxidantsCheckpoint Kinase 1Cyclin-Dependent Kinase Inhibitor p27DNA-Binding ProteinsDNA DamageDNA Repair EnzymesG1 Phase Cell Cycle CheckpointsGADD45 ProteinsHT29 CellsHumansIntracellular Signaling Peptides and ProteinsMicroscopy, Electron, ScanningNanotubesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Acid Anhydride HydrolasesAntioxidantsCheckpoint Kinase 1Cyclin-Dependent Kinase Inhibitor p27DNA-Binding ProteinsDNA Repair EnzymesGADD45 ProteinsIntracellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2RAD50 protein, humanTitaniumtitanium dioxideTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28337249
PMCPMC5350423
OpenAlexW2594684194

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.