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2014 ; 63
(6
): 881-90
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Long non-coding RNA HNF1A-AS1 regulates proliferation and migration in
oesophageal adenocarcinoma cells
#MMPMID24000294
Yang X
; Song JH
; Cheng Y
; Wu W
; Bhagat T
; Yu Y
; Abraham JM
; Ibrahim S
; Ravich W
; Roland BC
; Khashab M
; Singh VK
; Shin EJ
; Yang X
; Verma AK
; Meltzer SJ
; Mori Y
Gut
2014[Jun]; 63
(6
): 881-90
PMID24000294
show ga
OBJECTIVES: Long non-coding RNAs (lncRNA) have been shown to play important roles
in the development and progression of cancer. However, functional lncRNAs and
their downstream mechanisms are largely unknown in the molecular pathogenesis of
oesophageal adenocarcinoma (EAC) and its progression. DESIGN: lncRNAs that are
abnormally upregulated in EACs were identified by RNA-sequencing analysis,
followed by quantitative RT-PCR (qRTPCR) validation using tissues from 25 EAC
patients. Cell biological assays in combination with small interfering
RNA-mediated knockdown were performed in order to probe the functional relevance
of these lncRNAs. RESULTS: We discovered that a lncRNA, HNF1A-AS1, is markedly
upregulated in human primary EACs relative to their corresponding normal
oesophageal tissues (mean fold change 10.6, p<0.01). We further discovered that
HNF1A-AS1 knockdown significantly inhibited cell proliferation and
anchorage-independent growth, suppressed S-phase entry, and inhibited cell
migration and invasion in multiple in vitro EAC models (p<0.05). A gene
ontological analysis revealed that HNF1A-AS1 knockdown preferentially affected
genes that are linked to assembly of chromatin and the nucleosome, a mechanism
essential to cell cycle progression. The well known cancer-related lncRNA, H19,
was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this
finding, there was a significant positive correlation between HNF1A-AS1 and H19
expression in primary EACs (p<0.01). CONCLUSIONS: We have discovered abnormal
upregulation of a lncRNA, HNF1A-AS1, in human EAC. Our findings suggest that
dysregulation of HNF1A-AS1 participates in oesophageal tumorigenesis, and that
this participation may be mediated, at least in part, by modulation of chromatin
and nucleosome assembly as well as by H19 induction.
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