SRA

Purpose: To fully realize the potential molecular mechanism that S100A14 deficiency enhances esophageal carcinogenesis Methods: Total RNA of esophageal tumors in 4NQO WT and 4NQO S100A 14 CKO group mice was extracted with TRIzol Reagent. RNA libraries were constructed using an Illumina TruSeq RNA Sample Preparation kit according to the manufacturer's protocol. A total of 150 base paired-end reads were sequenced using the Novaseq 6000 S4 platform. The read alignment was conducted using TopHat 2.0.13, and relative transcript abundances and differentially expressed genes were determined using the DESeq R package. Results: We identified 14,157 transcripts in esophageal tumors of 4NQO WT and 4NQO S100A14 CKO group mice. Approximately 8% of the transcripts showed differential expression between the esophageal tumors of 4NQO WT and 4NQO S100A 14 CKO group mice, with a fold change =1.0 and p value <0.05. Conclusions: Our study represents the first analysis of esophageal tumors derived from S100A14 CKO mice with biologic replicates, generated by RNA-seq. Overall design: mRNA profiles of 4NQO induced-esophageal tumors of Wild Type and S100A14 CKO mice