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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	anaplastic thyroid cancer
ICD-0-3	C73
Methods	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown
Sample	anaplastic thyroid cancer tissues, cell lines (Nthy-ori3-1, SW1736 and KAT-18)
Expression Pattern	up-regulated
Function Description	The present study identified that the expression levels of UCA1, in ATC cell lines and tissues, were significantly upregulated compared with normal human thyroid cell line and adjacent non-cancerous tissues, respectively. UCA1 knockdown significantly inhibited ATC cell viability, proliferation, migration and invasion and the expression level of c-myc proto-oncogene (c-myc) in vitro, and suppressed ATC tumor growth in vivo. In addition, using luciferase assays, it was confirmed that miR-135a directly bound to UCA1 and the 3' untranslated region of c-myc, and UCA1 competed with c-myc for miR-135a binding. miR-135a inhibition may upregulate c-myc expression, however, the upregulation of c-myc may be partially reduced by short hairpin UCA1. The present results illustrated that UCA1 promoted ATC cell proliferation through acting as a competing endogenous RNA by binding miR-135a.
Pubmed ID	30015867
Year	2018
Title	Long Noncoding RNA UCA1 Promotes Anaplastic Thyroid Cancer Cell Proliferation via miR-135a-mediated C-myc Activation

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