Human　papillomavirus　(HPV)　infection　is　one　of　the　main　causes　of　esophageal　carcinoma　(ESCA),　and　its　carcinogenic　mechanisms　in　ESCA　require　further　investigation.　E6　and　E7　are　HPV　oncogenes,　and　their　genomic　integration　is　a　crucial　reason　for　the　transformation　of　host　cells　into　cancer　cells.　In　order　to　reveal　the　role　of　oncogenes　E6　and　E7　in　ESCA　cells,　the　RNA-Seq　raw　data　for　HPV18-positive　and　-negative　esophageal　squamous　cell　carcinoma　(ESCC)　samples　derived　from　the　NCBI　BioProject　database　were　analyzed,　and　the　differentially　expressed　genes　were　identified.　Moreover,　differentially　expressed　genes　were　enriched　significantly　in　multiple　cell　death　pathways,　including　apoptosis　(cyclin-dependent　kinase　inhibitor　2A,　plakophilin　1　and　desmoglein　3),　pyroptosis　(gasdermin　A,　gasdermin　C,　NLR　family　pyrin　domain　containing　3,　absent　in　melanoma　2,　NLR　family　pyrin　domain　containing　1　and　Toll　like　receptor　1)　and　autophagy　(Unc-51　like　autophagy　activating　kinase　1,　adrenoceptor　beta　2).　Consequently,　the　effects　of　cisplatin-induced　apoptosis　and　Hank＇s　balanced　salt　solution-induced　autophagy,　and　alpha-ketoglutarate-induced　pyroptosis　in　the　ESCC-expressing　E6　and　E7　cells　were　verified.　Therefore,　the　expression　of　E6E7　may　culminate　in　the　inhibition　of　multiple　cell　death　modes,　which　may　also　be　one　of　the　mechanisms　of　oncogene-induced　carcinogenesis.