MiR-486-5p negatively regulates oncogenic NEK2 in hepatocellular carcinoma

Shun Jun Fu, Jian Chen, Fei Ji, Wei Qiang Ju, Qiang Zhao, Mao Gen Chen, Zhi Yong Guo, Lin Wei Wu, Yi Ma, Dong Ping Wang, Xiao Feng Zhu, Xiao Shun He

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

NEK2 is a member of the NIMA-related family of serine/threonine centrosomal kinases. We analyzed the relationship between differential expression of NEK2 and hepatocellular carcinoma (HCC) patient outcomes after liver transplants. We also studied the microRNAs that affect NEK2 expression. Analysis of multiple microarrays in the Oncomine database revealed that NEK2 expression was higher in HCC tissues than adjacent normal liver tissues. High NEK2 expression correlated with tumor size, pathological grade and macro- and microvascular invasion. Consequently, patients exhibiting high NEK2 expression had poorer prognosis. This was corroborated by our multivariate analysis that showed NEK2 to be an independent prognostic factor for HCC patient survival. Further, high NEK2 expression promoted proliferation, colony formation, migration and invasion of HCC cell lines. Tumor xenograft data from Balb/c nude mice demonstrated that HCC cells with high NEK2 expression formed larger tumors than those with low NEK2 expression. Finally, we showed that miR-486-5p suppressed NEK2 by directly binding to its transcript 3’UTR. We also demonstrated an inverse relationship between miR-486-5p and NEK2 expression in HCC patients. These findings suggest miR-486-5p negatively regulates NEK2, which is a critical prognostic indicator of HCC patient survival after liver transplantation.

Original languageEnglish (US)
Pages (from-to)52948-52959
Number of pages12
JournalOncotarget
Volume8
Issue number32
DOIs
StatePublished - May 5 2017

Keywords

  • Hepatocellular carcinoma
  • MiR-486-5p
  • NEK2
  • Prognosis
  • Tumor progression

ASJC Scopus subject areas

  • Oncology

Fingerprint Dive into the research topics of 'MiR-486-5p negatively regulates oncogenic NEK2 in hepatocellular carcinoma'. Together they form a unique fingerprint.

Cite this