A transcriptomic analysis of malignant transformation of human embryonic esophageal epithelial cells by HPV18 E6E7.

Background: Esophageal cancer is one of the most common malignant tumours in humans. A series of esophageal cancer cell lines are accompanied by human papilloma virus (HPV) infection, but the mechanism behind HPV in cancer malignancy is not clear.

Methods: This research was conducted in different generations of HPV E6E7 gene-induced human foetal esophageal epithelial immortalised cells (Shantou Human Embryonic Esophageal Epithelial cell line; SHEE); the RNA sequencing transcriptomic analysis was performed to explore the mechanism of HPV infection in these cell lines.

Results: The results showed that there are 9,990 differential genes in late-stage cells compared with HPV18 E6E7-infected early foetal esophageal epithelial immortalised cells. Among these, 4,882 genes are upregulated, and 5,108 genes are downregulated. We used bioinformatics to analyze the expression and function of aberrantly expressed lncRNA, miRNA, mRNA and construct the competing endogenous RNA (ceRNA) network and protein protein interaction (PPI) network.

Conclusions: we predicted TP53TG1 promotes to malignant transformation of SHEEs by acting as a ceRNA to competitively bind to miR-6835 and regulate IGF2 expression. We also predicted IL6 serve as prognostic biomarkers and therapy target. With these results maybe provides new insights into the mechanisms of HPV carcinogenesis in esophageal cancer.