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Knockdown of lncRNA MIR31HG inhibits cell proliferation in human HaCaT keratinocytes

dc.creatorGao,Jintao
dc.creatorChen,Fangru
dc.creatorHua,Mingchun
dc.creatorGuo,Junfan
dc.creatorNong,Yuejuan
dc.creatorTang,Qinyan
dc.creatorZhong,Fengxia
dc.creatorQin,Linxiu
dc.date2018-01-01
dc.date.accessioned2019-05-02T21:22:43Z
dc.date.available2019-05-02T21:22:43Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100226
dc.identifier.urihttp://revistaschilenas.uchile.cl/handle/2250/82765
dc.descriptionAbstract 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.
dc.formattext/html
dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.1186/s40659-018-0181-8
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.51 2018
dc.subjectKnockdown
dc.subjectLncRNA
dc.subjectMIR31HG
dc.subjectProliferation
dc.subjectHaCaT keratinocytes
dc.titleKnockdown of lncRNA MIR31HG inhibits cell proliferation in human HaCaT keratinocytes


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