We performed HNF4α chromatin immunoprecipitation followed by sequencing across multiple GC cell lines, integrating HNF4α occupancy data with (epi)genomic and transcriptome data of primary GCs to define HNF4α target genes of <i>in vitro</i> and <i>in vivo</i> relevance.
In conclusion, the results of the present study indicate the involvement of TFs in MDR in GC, and suggest that HNF-4α may enhance MDR in GC by regulating cell apoptosis and Bcl-2 expression.
Our results indicate that HNF4α is a targetable oncoprotein in GC, is regulated by AMPK signalling through AMPKα and resides upstream of WNT signalling.
Taken together, these data indicate that ITLN1 suppresses the progression of gastric cancer through up-regulation of HNF4α, and is associated with improved survival in patients with gastric cancer.
We conclude that the pCOX2-0.8 minimal promoter contains a novel functional T-cell factor/lymphoid enhancer factor (TCF/LEF)-response element (TBE Site II; -689/-684) that responds directly to enhanced Wnt/β-catenin signaling and which may be important for the onset/progression of GC.
It has been reported that the dysregulation of hepatocyte nuclear factor-4alpha (HNF4alpha) expression is linked to the development of CRC, gastric cancer and hepatocellular carcinoma.