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Basic Information

Classification Information

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

Cancer&Entry Information

Cancer Name	osteosarcoma
ICD-0-3	NA
Methods	qPCR, Western blot, Luciferase reporter assay, RIP, etc.
Sample	Osteosarcoma (OS) tissues, Human osteosarcoma cell lines (MG-63, MNNG/HOS, U2OS, 143B) and the human osteoblast cell hFOB1.19
Expression Pattern	up-regulated
Function Description	At first, we measured the high expression of MIR100HG in OS tissues and cell lines by qRT-PCR. Kaplan-Meier method revealed that high expression of MIR100HG is a factor for the poor prognosis of OS patients (P=0.004). To explore the effect of MIR100HG on the biological processes of OS, loss-of-function assays were conducted in OS cells. Functionally, MIR100HG knockdown suppressed cell proliferation, cell cycle progression while promoted cell apoptosis. Mechanistically, MIR100HG was upregulated by the transcription factor ELK1. The upregulation of MIR100HG led to the inactivation of Hippo pathway. Furthermore, we found that MIR100HG inactivated Hippo pathway in OS cells by epigenetically silencing LATS1 and LATS2. Rescue assays demonstrated that LATS1/2 involved in MIR100HGmediated OS progression. In summary, our study indicated that ELK1-induced upregulation of MIR100HG promoted OS progression by epigenetically silencing LATS1 and LATS2 and inactivating Hippo pathway.
Pubmed ID	30551532
Year	2019
Title	ELK1-induced Upregulation of Long Non-Coding RNA MIR100HG Predicts Poor Prognosis and Promotes the Progression of Osteosarcoma by Epigenetically Silencing LATS1 and LATS2

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