Knockdown of lncRNA MIR31HG inhibits cell proliferation in human HaCaT keratinocytes

被引:39
作者
Gao, Jintao [1 ]
Chen, Fangru [2 ]
Hua, Mingchun [3 ]
Guo, Junfan [1 ]
Nong, Yuejuan [1 ]
Tang, Qinyan [1 ]
Zhong, Fengxia [1 ]
Qin, Linxiu [1 ]
机构
[1] Guilin Med Univ, Coll Biotechnol, Guilin 541100, Guangxi, Peoples R China
[2] Guilin Med Univ, Affiliated Hosp, Dept Dermatol, Guilin 541001, Guangxi, Peoples R China
[3] Guilin Med Univ, Affiliated Hosp, Dept Plast Surg, Guilin 541001, Guangxi, Peoples R China
关键词
Knockdown; LncRNA; MIR31HG; Proliferation; HaCaT keratinocytes; LONG NONCODING RNAS; HYPERPROLIFERATION-ASSOCIATED KERATINS; HEALTHY SKIN; PSORIASIS; DISEASE; GROWTH; PRINS; K16;
D O I
10.1186/s40659-018-0181-8
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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-kappa B activation. Conclusions: NF-kappa B 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.
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页数:7
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