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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	esophageal squamous cell carcinoma
ICD-0-3	NA
Methods	RNA-seq, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP
Sample	esophageal squamous cell carcinoma (ESCC) tissues and cell lines (KYSE150 and KYSE510)
Expression Pattern	up-regulated
Function Description	Both in vivo and in vitro studies revealed that EZR-AS1 promoted cell migration through up-regulation of EZR expression. Mechanistically, antisense lncRNA EZR-AS1 formed a complex with RNA polymerase II to activate the transcription of EZR. Moreover, EZR-AS1 could recruit SMYD3 to a binding site, present in a GC-rich region downstream of the EZR promoter, causing the binding of SMYD3 and local enrichment of H3K4me3. Finally, the interaction of EZR-AS1 with SMYD3 further enhanced EZR transcription and expression. Our findings suggest that antisense lncRNA EZR-AS1, as a member of an RNA polymerase complex and through enhanced SMYD3-dependent H3K4 methylation, plays an important role in enhancing transcription of the EZR gene to promote the mobility and invasiveness of human cancer cells.EZR-AS1 regulates EZR transcriptional activity in ESCC cells by interacting with RNA polymerase II, but not by affecting the binding of SP1 and AP-1 transcription factors. the overexpression of EZR-AS1 accompanied the enhanced expression of EZR (variant 1), both at the mRNA and protein levels, in KYSE150 cells (Figure 1H and I).
Pubmed ID	29253179
Year	2018
Title	The interaction of lncRNA EZR-AS1 with SMYD3 maintains overexpression of EZR in ESCC cells.

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