Research Papers:

Comprehensive analysis of lncRNAs microarray profile and mRNA–lncRNA co-expression in oncogenic HPV-positive cervical cancer cell lines

LingYun Yang, Ke Yi, HongJing Wang, YiQi Zhao and MingRong Xi _

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Oncotarget. 2016; 7:49917-49929. https://doi.org/10.18632/oncotarget.10232

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LingYun Yang1, Ke Yi1, HongJing Wang1, YiQi Zhao1, MingRong Xi1

1Department of Gynecology and Obstetrics, West China Second University Hospital, Sichuan University, Chengdu 610041, China

Correspondence to:

MingRong Xi, email: [email protected]

Keywords: lncRNA, expression profile, coding non-coding gene co-expression, oncogenic HPV, cervical cancer

Received: February 07, 2016     Accepted: May 16, 2016     Published: June 23, 2016


Long non-coding RNAs are emerging to be novel regulators in gene expression. In current study, lncRNAs microarray and lncRNA-mRNA co-expression analysis were performed to explore the alternation and function of lncRNAs in cervical cancer cells. We identified that 4750 lncRNAs (15.52%) were differentially expressed in SiHa (HPV-16 positive) (2127 up-regulated and 2623 down-regulated) compared with C-33A (HPV negative), while 5026 lncRNAs (16.43%) were differentially expressed in HeLa (HPV-18 positive) (2218 up-regulated and 2808 down-regulated) respectively. There were 5008 mRNAs differentially expressed in SiHa and 4993 in HeLa, which were all cataloged by GO terms and KEGG pathway. With the help of mRNA-lncRNA co-expression network, we found that ENST00000503812 was significantly negative correlated with RAD51B and IL-28A expression in SiHa, while ENST00000420168, ENST00000564977 and TCONS_00010232 had significant correlation with FOXQ1 and CASP3 expression in HeLa. Up-regulation of ENST00000503812 may inhibit RAD51B and IL-28A expression and result in deficiency of DNA repair pathway and immune responses in HPV-16 positive cervical cancer cell. Up-regulation of ENST00000420168, ENST00000564977 and down-regulation of TCONS_00010232 might stimulate FOXQ1 expression and suppress CASP3 expression in HPV-18 positive cervical cancer cell, which lead to HPV-induced proliferation and deficiency in apoptosis. These results indicate that changes of lncRNAs and related mRNAs might impact on several cellular pathways and involve in HPV-induced proliferation, which enriches our understanding of lncRNAs and coding transcripts anticipated in HPV oncogenesis of cervical cancer.

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