Long non-coding RNA XIST promotes cell growth by regulating miR-139-5p/PDK1/AKT axis in hepatocellular carcinoma

Abnormal expression of long non-coding RNA often contributes to unrestricted growth of cancer cells. Long non-coding RNA XIST expression is upregulated in several cancers; however, its modulatory mechanisms have not been reported in hepatocellular carcinoma. In this study, we found that XIST express...

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Bibliographic Details
Published in:Tumor biology 2017-02, Vol.39 (2), p.1010428317690999
Main Authors: Mo, Yichao, Lu, Yaoyong, Wang, Peng, Huang, Simin, He, Longguang, Li, Dasheng, Li, Fuliang, Huang, Junwei, Lin, Xiaoxia, Li, Xueru, Che, Siyao, Chen, Qinshou
Format: Article
Language:English
Subjects:
AKT protein
Animals
Apoptosis
Cancer therapies
Carcinoma, Hepatocellular - genetics
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
Case-Control Studies
Cell cycle
Cell growth
Cell Line, Tumor
Cell lines
Cell proliferation
G1 phase
Hep G2 Cells
Hepatocellular carcinoma
Humans
Kinases
Liver cancer
Liver Neoplasms - genetics
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Male
Metastasis
Mice
Mice, Inbred BALB C
MicroRNAs
MicroRNAs - genetics
MicroRNAs - metabolism
Non-coding RNA
Polymerase chain reaction
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - metabolism
Proteins
Proto-Oncogene Proteins c-akt - genetics
Proto-Oncogene Proteins c-akt - metabolism
RNA, Long Noncoding - biosynthesis
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
S phase
Signal transduction
Stem cells
Tissues
Tumor cell lines
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Summary:Abnormal expression of long non-coding RNA often contributes to unrestricted growth of cancer cells. Long non-coding RNA XIST expression is upregulated in several cancers; however, its modulatory mechanisms have not been reported in hepatocellular carcinoma. In this study, we found that XIST expression was significantly increased in hepatocellular carcinoma tissues and cell lines. XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to hepatocellular carcinoma cell growth. In addition, we revealed that there was reciprocal repression between XIST and miR-139-5p. PDK1 was identified as a direct target of miR-139-5p. We proposed that XIST was responsible for hepatocellular carcinoma cell proliferation, and XIST exerted its function through the miR-139-5p/PDK1 axis.
ISSN:1010-4283
1423-0380
DOI:10.1177/1010428317690999