LncRNA TUG1 interacting with miR-144 contributes to proliferation, migration and tumorigenesis through activating the JAK2/STAT3 pathway in hepatocellular carcinoma

Jun Lv; Yongkui Kong; Zhiqiang Gao; Yanmin Liu; Pengfei Zhu; Zujiang Yu

doi:10.1016/j.biocel.2018.05.010

LncRNA TUG1 interacting with miR-144 contributes to proliferation, migration and tumorigenesis through activating the JAK2/STAT3 pathway in hepatocellular carcinoma

Int J Biochem Cell Biol. 2018 Aug:101:19-28. doi: 10.1016/j.biocel.2018.05.010. Epub 2018 May 20.

Authors

Jun Lv¹, Yongkui Kong², Zhiqiang Gao³, Yanmin Liu¹, Pengfei Zhu⁴, Zujiang Yu⁵

Affiliations

¹ Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, PR China.
² Department of Blood Transfusion, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, PR China.
³ Department of Hepatobiliary Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, PR China.
⁴ Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, PR China. Electronic address: [email protected].
⁵ Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, PR China. Electronic address: [email protected].

PMID: 29791864
DOI: 10.1016/j.biocel.2018.05.010

Abstract

Recently, it is reported that taurine upregulated gene 1 (TUG1) participates in the tumor progression by acting as a competing endogenous RNA (ceRNA) of miRNAs. Nonetheless, whether TUG1 could serve as a ceRNA of miR-144 in hepatocellular carcinoma (HCC) progression remains undefined. Here, our results indicated that there was a marked rise in TUG1 expression in HCC tissues and cells, and downregulation of TUG1 hindered proliferation and migration of HCC cells. Additionally, TUG1 was validated to act as a molecular sponge of miR-144. Furthermore, we found that TUG1 interacting with miR-144 contributed to proliferation and migration of HCC cells via activating the JAK2/STAT3 pathway in vitro. Moreover, TUG1 knockdown inhibited HCC tumor growth in vivo through upregulating miR-144 via inactivation of the JAK2/STAT3 pathway. In conclusion, TUG1 interacting with miR-144 contributed to proliferation, migration and tumorigenesis through activation of the JAK2/STAT3 pathway in HCC.

Keywords: Hepatocellular carcinoma; TUG1; The JAK2/STAT3 pathway; miR-144.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Base Sequence
Carcinogenesis / genetics
Carcinogenesis / metabolism
Carcinogenesis / pathology
Carcinoma, Hepatocellular / genetics*
Carcinoma, Hepatocellular / pathology
Carcinoma, Hepatocellular / surgery
Carcinoma, Hepatocellular / therapy
Cell Line, Tumor
Cell Movement
Cell Proliferation
Female
Gene Expression Regulation, Neoplastic*
Genes, Reporter
Hep G2 Cells
Humans
Janus Kinase 2 / genetics*
Janus Kinase 2 / metabolism
Liver Neoplasms / genetics*
Liver Neoplasms / pathology
Liver Neoplasms / surgery
Liver Neoplasms / therapy
Luciferases / genetics
Luciferases / metabolism
Mice
Mice, Nude
MicroRNAs / genetics*
MicroRNAs / metabolism
RNA, Long Noncoding / antagonists & inhibitors
RNA, Long Noncoding / genetics*
RNA, Long Noncoding / metabolism
RNA, Small Interfering / genetics
RNA, Small Interfering / metabolism
STAT3 Transcription Factor / genetics*
STAT3 Transcription Factor / metabolism
Signal Transduction
Xenograft Model Antitumor Assays

Substances

MIRN144 microRNA, human
MicroRNAs
RNA, Long Noncoding
RNA, Small Interfering
STAT3 Transcription Factor
STAT3 protein, human
TUG1 long noncoding RNA, human
Luciferases
JAK2 protein, human
Janus Kinase 2