Long non-coding RNA DICER1-AS1-low expression in arsenic-treated A549 cells inhibits cell proliferation by regulating the cell cycle pathway

•Inorganic arsenic, not MMA and DMA, inhibited the expression of DICER1-AS1.•DICER1-AS1 silencing could decrease proliferation in the A549 cell.•DICER1-AS1 regulated the expression of p21, Cyclin A2, Cyclin E2, CDK1 and PCNA. Arsenic, an environmental pollution with diverse toxicities, incurs public...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Environmental toxicology and pharmacology 2021-05, Vol.84, p.103617, Article 103617
Hauptverfasser: Jiang, Chenglan, Sun, Mingjun, Li, Shuting, Tan, Jingwen, Wang, Mengjie, He, Yuefeng
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:•Inorganic arsenic, not MMA and DMA, inhibited the expression of DICER1-AS1.•DICER1-AS1 silencing could decrease proliferation in the A549 cell.•DICER1-AS1 regulated the expression of p21, Cyclin A2, Cyclin E2, CDK1 and PCNA. Arsenic, an environmental pollution with diverse toxicities, incurs public health problems. Arsenic trioxide could inhibit cell proliferation in vitro experiments, but the underlying mechanisms are not fully known. LncRNAs are also involved in the arsenic-induced toxicological responses. In our study, we found that the expression of lncRNA DICER1-AS1 was significantly inhibited by sodium arsenite in a dose-dependent manner. DICER1-AS1 silencing decreased the A549 cell proliferation and inhibited cell cycle progression. Importantly, DICER1-AS1 silencing induced upregulation of p21 and downregulation of Cyclin A2, Cyclin E2, CDK1 and PCNA. In conclusion, our study provided a new lncRNA-dictated regulatory mechanism participating in arsenic-induced inhibition of cell proliferation.
ISSN:1382-6689
1872-7077
DOI:10.1016/j.etap.2021.103617