Long non-coding nuclear paraspeckle assembly transcript 1 acts as prognosis biomarker and increases cell growth and invasion in cervical cancer by sequestering microRNA-101

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Abstract

Emerging studies have focused on the essential role of long non-coding RNAs (lncRNAs) in cervical carcinogenesis. A recent study has indicated that nuclear paraspeckle assembly transcript 1 (NEAT1) is highly expressed in the human cervical tissue. However, whether NEAT1 is involved in cervical cancer remains to be elucidated. Reverse transcription-quantitative polymerase chain reaction results demonstrated that the expression of NEAT1 was higher in cervical cancer cells/tissues compared with that in normal human keratinocytes/tissues. Patients with higher NEAT1 level had poorer clinical characteristics and a shorter survival time compared with those that exhibited lower NEAT1 expression levels. In vitro, flow cytometery analysis revealed that transfection with NEAT1 small interfering RNA retarded cervical cancer cell (Caski and HeLa) growth by decreasing the percentage of S phase in the cell cycle and inducing cell apoptosis. In addition, the colony formation assay, wound healing assay and matrigel invasion assay results indicated that downregulation of NEAT1 inhibited colony formation, cell migration and invasion. Further investigation using the luciferase reporter assay revealed that the expression of mircoRNA-101 (miR-101) target gene Fos was positively associated with NEAT1 expression due to NEAT1-competitive molecular sequestering of miR-101 via base pairing. Furthermore, reduction of miR-101 expression by inhibitor transfection reversed the effect of NEAT1 siRNA on cervical cancer cells. To conclude, the present data indicated that NEAT1 promoted cervical cancer progression by targeting miR-101.

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Wang, L., & Zhu, H. (2018). Long non-coding nuclear paraspeckle assembly transcript 1 acts as prognosis biomarker and increases cell growth and invasion in cervical cancer by sequestering microRNA-101. Molecular Medicine Reports, 17(2), 2771–2777. https://doi.org/10.3892/mmr.2017.8186

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