HPV 16 E6 promotes growth and metastasis of esophageal squamous cell carcinoma cells in vitro

Abstract

BackgroundEsophageal squamous cell carcinoma (ESCC) is one of the most lethal malignancies. Increasing evidence has revealed that Human Papillomavirus (HPV) infection may be associated with the possible etiology of ESCC. Nevertheless, the precise role of HPV in ESCC remains unclear. MethodsProliferation and apoptosis capability of ESCC cells upon infection of HPV16 E6 were detected by CCK-8 assay and Western blotting analysis. Wound healing assay and Transwell experiment were conducted to determine the ability of migration and invasion, and the mRNA expression of E6AP, p53, miR-34a was determined by real-time PCR after transfected with HPV16 E6 plasmid. ResultsIn ESCC cells, the ability of proliferation, migration and invasion were increased, and the ability of apoptosis was decreased after transfected with HPV16 E6 plasmid. Furthermore, the mRNA level of E6AP, P53 and miR-34a were decreased in HPV16 E6-transfected cell lines. ConclusionsOur results not only provide evidence that in ESCC, HPV16 E6 promotes cell proliferation, migration and invasion, inhibits cell apoptosis, but also suggest that there may be a correlation between E6AP, P53 and miR-34a in HPV-transfected cell lines. These ndings indicated that HPV16 E6 may play an important role in the development of ESCC.

HPV16 infection promotes the malignant transformation of the esophagus and progression of esophageal squamous cell carcinoma

“…After ESCC formation, the HPV16 E6 and E7 genes still contribute to the following malignant processes, including proliferation, migration, invasion and tumorigenesis, and the result of the HPV16 E6 gene in ESCC cells is partly consistent with previous results from other ESCC cells 44 . Even in some malignant processes, the E6 and E7 genes have synergistic effects, such as the growth of ESCC cells in vivo.…”

“…After ESCC formation, the HPV16 E6 and E7 genes still contribute to the following malignant processes, including proliferation, migration, invasion and tumorigenesis, and the result of the HPV16 E6 gene in ESCC cells is partly consistent with previous results from other ESCC cells. 44 Even in some malignant processes, the E6 and E7 genes have synergistic effects, such as the growth of ESCC cells in vivo. After RNA sequencing and proteomic assays, we found that some apoptotic and proliferation processes, including the p53 signaling pathway and MAPK pathway, were enriched upon overexpression of the HPV E6 and E7 genes, which is also partly consistent with a previous study.…”