Hypothesis: Long non-coding RNA is a potential target of mycotoxins
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, přehledy
PubMed
34246706
DOI
10.1016/j.fct.2021.112397
PII: S0278-6915(21)00430-0
Knihovny.cz E-zdroje
- Klíčová slova
- Long non-coding RNA, Mycotoxins, Oxidative stress, Target, Toxicity mechanism,
- MeSH
- apoptóza účinky léků MeSH
- autofagie účinky léků MeSH
- lidé MeSH
- mykotoxiny farmakologie MeSH
- nádorové buněčné linie MeSH
- oxidační stres účinky léků MeSH
- RNA dlouhá nekódující metabolismus MeSH
- únik nádoru z imunitní kontroly účinky léků MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- mykotoxiny MeSH
- RNA dlouhá nekódující MeSH
The molecular target of mycotoxins is not fully understood. Extensive data derived from cell and animal experimental studies demonstrate that long non-coding RNAs (lncRNAs) play crucial roles in mycotoxin-induced toxicities. Mycotoxins stimulate the upregulation/downregulation of lncRNA expression, which further promote apoptosis, is related to the mTOR/FoxO signaling pathway, and contributes to tumor cell growth, death, and liver and chondrocyte damage. Moreover, lncRNA can establish interactions with NF-κB and cause immune evasion. These preliminary data suggest that lncRNAs are involved in potential upstream regulatory events and further regulate downstream apoptosis, oxidative stress, and anti-apoptotic events that affect cell death and survival. Therefore, we hypothesize that lncRNAs are potential targets of mycotoxins. Investigation of the expression of the potential target lncRNAs by mycotoxin-mediated stimulation, and exploration of the upstream and downstream relationship between lncRNA and the key proteins involved in mycotoxin toxicity, should be performed. This Hypothesis provides clues for further understanding of the molecular mechanisms of mycotoxins.
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