HOXA13 in etiology and oncogenic potential of Barrett’s esophagus. Janmaat et al.
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Datasets relate to several sub-sections of the results section of the paper: "HOXA13 in etiology and oncogenic potential of Barrett’s esophagus", Janmaat et al. 1) Forced HOXA13 confers a relative competitive advantage in multipotent cell cultures through upregulation of Nanog signaling and downregulation of Wnt signaling (Figure 6; Table 1). 2) Forced HOXA13 expression supports caudal epithelial functions and promotes proliferation in definitive endoderm (Table 1; Table S1; Extended data file S2). 3) HOXA13 downregulates the chromosome 1 epidermal differentiation complex and is pro-oncogenic (Figure 7; Table 1; Extended data file S3). See the paper for details.
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RNA-Sequencing The EPC2-hTERT samples (n=8) were treated with the TruSeq Stranded mRNA Library Prep Kit. Sequencing took place according to the Illumina TruSeq v3 protocol on an Illumina HiSeq2500 sequencer. Sample preparation and sequencing were performed at the Erasmus MC in Rotterdam, The Netherlands. Reads of 50 base-pairs were generated and mapped against reference genome hg19 with Tophat (version 2.0.10). Expression was quantified using HTseq-count (0.6.1). Stranded libraries of the BAR-T (n=6), and both nondifferentiated and differentiated KH2 mESCs (n=6 each) were prepared with the NEBNext RNA Ultra sample prep kit. Sequencing took place according to the Illumina NestSeq 500 protocol on an Illumina HiSeq2500 sequencer. Sample preparation and sequencing was performed at GenomeScan in Leiden, The Netherlands. Reads of 75 base-pairs were generated, mapped against reference genome hg19 or mm9 with Tophat (version 2.1.0), and quantified using HTSeq (version 0.6.1p1). Data were processed using R. version 3.2.5, (R Development Core Team, 2008) in combination with the module DeSeq2 (Love et al., 2014).