TY - JOUR
T1 - High expression of long non-coding HOTAIR correlated with hepatocarcinogenesis and metastasis
AU - Zhong, Da Ni
AU - Luo, Yi Huan
AU - Mo, Wei Jia
AU - Zhang, Xin
AU - Tan, Zhong
AU - Zhao, Na
AU - Pang, Si Min
AU - Chen, Gang
AU - Rong, Min Hua
AU - Tang, Wei
PY - 2018/1
Y1 - 2018/1
N2 - HOX transcript antisense RNA (HOTAIR), a newly discovered long noncoding RNA (IncRNA), has been reported to be a poor prognostic marker in many types of cancers. The current study attempted to investigate the biological roles and clinicopathlogical implications of HOTAIR in hepatocellular carcinoma (HCC), as well as understand the molecular mechanisms of HOTAIR in HCC progression. HOTAIR expression in 95 HCC patients with paired HCC tissues and adjacent non-cancer tissues were investigated using quantitative reverse transcription-polymerase chain reaction. The association between HOTAIR expression and clinicopathological features was assessed. The effects of HOTAIR were examined in vitro assays by silencing the IncRNA. Pathway analyses were performed to illustrate the biological functions of the HOTAIR and coexpression genes. The expression level of HOTAIR was observed significantly higher in the HCC tissue than the adjacent non-tumor tissue. HOTAIR expression levels were significantly higher in tumor samples from patients with distant metastasis, advanced stage, portal vein tumor embolus, vasoinvasion, tumor capsular infiltration or positive nm23 expression than those from patients without these conditions, correspondingly. The silencing of HOTAIR in liver cancer cells induced the inhibition of cell proliferation and promotion of apoptosis. Several pathways such as extracellular matrix-receptor interaction, focal adhesion, pathways in cancer were annotated with the HOTAIR and coexpression genes. In summary, the present analysis indicates that HOTAIR might be an oncogene in HCC. It functions though promoting tumor cell growth and inhibiting apoptosis. HOTAIR may potentially be involved in HCC metastatic progression by several pathways correlated to cell adhesion, and may be a therapeutic target in future.
AB - HOX transcript antisense RNA (HOTAIR), a newly discovered long noncoding RNA (IncRNA), has been reported to be a poor prognostic marker in many types of cancers. The current study attempted to investigate the biological roles and clinicopathlogical implications of HOTAIR in hepatocellular carcinoma (HCC), as well as understand the molecular mechanisms of HOTAIR in HCC progression. HOTAIR expression in 95 HCC patients with paired HCC tissues and adjacent non-cancer tissues were investigated using quantitative reverse transcription-polymerase chain reaction. The association between HOTAIR expression and clinicopathological features was assessed. The effects of HOTAIR were examined in vitro assays by silencing the IncRNA. Pathway analyses were performed to illustrate the biological functions of the HOTAIR and coexpression genes. The expression level of HOTAIR was observed significantly higher in the HCC tissue than the adjacent non-tumor tissue. HOTAIR expression levels were significantly higher in tumor samples from patients with distant metastasis, advanced stage, portal vein tumor embolus, vasoinvasion, tumor capsular infiltration or positive nm23 expression than those from patients without these conditions, correspondingly. The silencing of HOTAIR in liver cancer cells induced the inhibition of cell proliferation and promotion of apoptosis. Several pathways such as extracellular matrix-receptor interaction, focal adhesion, pathways in cancer were annotated with the HOTAIR and coexpression genes. In summary, the present analysis indicates that HOTAIR might be an oncogene in HCC. It functions though promoting tumor cell growth and inhibiting apoptosis. HOTAIR may potentially be involved in HCC metastatic progression by several pathways correlated to cell adhesion, and may be a therapeutic target in future.
KW - Hepatocellular carcinoma
KW - HOTAIR
KW - Metastasis
KW - Oncogene
KW - Progression
UR - http://www.scopus.com/inward/record.url?scp=85035034106&partnerID=8YFLogxK
U2 - 10.3892/mmr.2017.7999
DO - 10.3892/mmr.2017.7999
M3 - Article
C2 - 29115524
AN - SCOPUS:85035034106
SN - 1791-2997
VL - 17
SP - 1148
EP - 1156
JO - Molecular Medicine Reports
JF - Molecular Medicine Reports
IS - 1
ER -