SciELO - Scientific Electronic Library Online

 
vol.51Contributions to the bryological knowledge of ASPA 125, Fildes Peninsula, King George IslandmiR-214 ameliorates acute kidney injury via targeting DKK3 and activating of Wnt/β-catenin signaling pathway índice de autoresíndice de materiabúsqueda de artículos
Home Pagelista alfabética de revistas  

Servicios Personalizados

Revista

Articulo

Indicadores

Links relacionados

  • En proceso de indezaciónCitado por Google
  • No hay articulos similaresSimilares en SciELO
  • En proceso de indezaciónSimilares en Google

Compartir


Biological Research

versión impresa ISSN 0716-9760

Resumen

GAO, Jintao et al. Knockdown of lncRNA MIR31HG inhibits cell proliferation in human HaCaT keratinocytes. Biol. Res. [online]. 2018, vol.51, 30.  Epub 15-Oct-2018. ISSN 0716-9760.  http://dx.doi.org/10.1186/s40659-018-0181-8.

Background:

Psoriasis is a complex, chronic inflammatory skin disease with substantial negative effects on patient quality of life. Long non-coding RNAs (lncRNAs) are able to be involved in multitudes of cellular processes in diverse human diseases. This study aimed to investigate the potential involvement of lncRNA MIR31HG in HaCaT keratinocytes proliferation.

Results:

The study showed that MIR31HG was significantly elevated in the lesional psoriatic skin compared with normal individuals’ skin. Knockdown of MIR31HG inhibited HaCaT keratinocytes proliferation. Flow cytometry analysis showed that siRNA-mediated MIR31HG depletion induced cell cycle arrest in the G2/M phase. In addition, MIR31HG expression was found to be dependent on NF-κB activation.

Conclusions:

NF-κB activation mediated MIR31HG upregulation plays an important role in the regulation of HaCaT keratinocytes proliferation. It could be a potential diagnostic biomarker and therapeutic target for psoriasis.

Palabras clave : Knockdown; LncRNA; MIR31HG; Proliferation; HaCaT keratinocytes.

        · texto en Inglés     · Inglés ( pdf )