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Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis		Drug
Variant		Cell Growth		Circulating
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	liver cancer
ICD-0-3	C22.0
Methods	qPCR, Western blot, Luciferase reporter assay
Sample	liver cancer tissues, cell lines (MHCC 97H, HepG2 and Hep3B)
Expression Pattern	up-regulated
Function Description	The expression of HOTAIR was upregulated in liver cancer tissues and 3 liver cancer cell lines. Inhibition of HOTAIR with HOTAIR small interfering (si) RNA lentiviral vectors significantly suppressed the cell proliferation of HepG2 cells, and downregulated the protein expression levels of two proliferation markers, Ki67 and proliferating cell nuclear antigen (PCNA). Furthermore, inhibition of HOTAIR induced G0/G1 cycle arrest by increasing the expression of p27 and decreasing the expression of cyclin D1. It was then predicted and verified that miR-217 was the target of HOTAIR. Expression of miR-217 was downregulated in liver cancer tissues and the 3 liver cancer cell lines. Further results revealed that inhibition of HOTAIR markedly upregulated the expression of miR-217 in HepG2 cells, and miR-217 inhibitor-induced reduction of miR-217 was significantly suppressed by HOTAIR inhibition. Furthermore, the increased cell proliferation and growth, the upregulated expression of Ki67 and PCNA, and the reduced G0/G1 cycle arrest induced by miR-217 inhibitor were partly rescued by inhibition of HOTAIR. Finally, the in vivo experiment indicated that HOTAIR inhibition suppressed tumorigenesis, including the smaller tumor volume and the reduced levels of Ki67.
Pubmed ID	29849802
Year	2018
Title	HOTAIR Contributes to the Growth of Liver Cancer via Targeting miR-217

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