Journal
FEBS LETTERS
Volume 590, Issue 12, Pages 1729-1738Publisher
WILEY
DOI: 10.1002/1873-3468.12220
Keywords
H3K4 methylation; lncRNA PAUPAR; uveal melanoma
Funding
- Scientific Research Program of the National Health and Family Planning Commission of China [201402014]
- National Natural Science Foundation of China [31470757, U1432117]
- Program for Professor of Special Appointment (Eastern Scholar) at the Shanghai Institutions of Higher Learning [1410000159]
- Shanghai PuJiang Program [13PJ1405700]
- SMC-ChenXing Yong Scholar Program
- Science and Technology Commission of Shanghai [14JC1404100, 14JC1404200, 14430723100, 16ZR1419600]
- Scientific Research Program of the National Health and Family Planning Commission of China [201402014]
- National Natural Science Foundation of China [31470757, U1432117]
- Program for Professor of Special Appointment (Eastern Scholar) at the Shanghai Institutions of Higher Learning [1410000159]
- Shanghai PuJiang Program [13PJ1405700]
- SMC-ChenXing Yong Scholar Program
- Science and Technology Commission of Shanghai [14JC1404100, 14JC1404200, 14430723100, 16ZR1419600]
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Uveal melanoma (UM) is the most common primary intraocular tumour in adults and has a high incidence. Nearly 50% of patients with UM develop metastases after diagnosis. Long noncoding RNAs (lncRNAs) are involved in both oncogenic and tumour suppression pathways. We show that lncRNA PAUPAR is present at low levels in UM tissues and cell lines and modulates the tumourigenesis of UM in vitro and in vivo. The ectopic expression of PAUPAR in UM cells revealed that PAUPAR acts as a necessary UM suppressor and induces the silencing of HES1 expression, which significantly reduces tumour metastasis. Mechanistically, PAUPAR modulates HES1 expression by inhibiting histone H3K4 methylation. These data support a role of this lncRNA as a novel therapeutic target in cancer prevention and treatment.
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