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2016 ; 7
(1
): 241-54
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Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by
up-regulating sphingosine kinase 1 (SPHK1)
#MMPMID26540633
Lu Z
; Xiao Z
; Liu F
; Cui M
; Li W
; Yang Z
; Li J
; Ye L
; Zhang X
Oncotarget
2016[Jan]; 7
(1
): 241-54
PMID26540633
show ga
Highly up-regulated in liver cancer (HULC) is a long non-coding RNA (lncRNA). We
found that HULC up-regulated sphingosine kinase 1 (SPHK1), which is involved in
tumor angiogenesis. Levels of HULC were positively correlated with levels of
SPHK1 and its product, sphingosine-1-phosphate (S1P), in patients HCC samples.
HULC increased SPHK1 in hepatoma cells. Chicken chorioallantoic membrane (CAM)
assays revealed that si-SPHK1 remarkably blocked the HULC-enhanced angiogenesis.
Mechanistically, HULC activated the promoter of SPHK1 in hepatoma cells through
the transcription factor E2F1. Chromatin immunoprecipitation (ChIP) and
electrophoretic mobility shift assay (EMSA) further showed that E2F1 was capable
of binding to the E2F1 element in the SPHK1 promoter. HULC increased the
expression of E2F1 in hepatoma cells and levels of HULC were positively
correlated with those of E2F1 in HCC tissues. Intriguingly, HULC sequestered
miR-107, which targeted E2F1 mRNA 3'UTR, by complementary base pairing.
Functionally, si-SPHK1 remarkably abolished the HULC-enhanced tumor angiogenesis
in vitro and in vivo. Taken together, we conclude that HULC promotes tumor
angiogenesis in liver cancer through miR-107/E2F1/SPHK1 signaling. Our finding
provides new insights into the mechanism of tumor angiogenesis.
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