The E6 and E7 oncoproteins of human papilloma virus (HPV) type 16 havebeen known to cooperatively induce the immortalization and transformation of primarykeratinocytes. We established an E7 transgenic mouse model to screen HPV-relatedbiomakers using the omics approach. The methods used to identify HPV-modulatedfactors were genomics analysis by microarray using the Affymetrix 430 2.0 arrayto screen E7-modulated genes, and proteomics analysis using nano-LC-ESI-MS/MSto screen E7-modulated proteins with the lung tissue of E7 transgenic mice. Accordingto omics data, cyclin B1, cyclin E2, topoisomerase IIα, calnexin, activated leukocytecell adhesion molecule CD166, actinin α1, diaphorase 1, gelsolin, platelet glycoprotein,and annexin A2 and A4 were up-regulated in the E7-Tg mice, while... proteoglycan4, sarcolipin, titin, vimentin, drep 1, troponin and cofilin-1 were down-regulated.We further confirmed the significance of differences between the expression levelsof the selected factors in E7-Tg and non-Tg mice by real-time PCR. Genes relatedto cancer cell adhesion, cell cycle and migration, proliferation and apoptosis,as well as to the intermediate filament network and to endoplasmic reticulum proteins,were selected. Taken together, the results suggest that the E7 oncogene modulatesthe expression levels of cell cycle-related (cyclin B1, cyclin E2) and cell adhesion-and migration-related (actinin α1, CD166) factors, which may play important rolesin cellular transformation in cancer. In addition, the solubilization of the rigidintermediate filament network by specific proteolysis mediated via up-regulatinggelsolin and down-regulating cofilin-1, as well as increased levels of endoplasmicreticulum protein calnexin with chaperone functions, might also be involved inE7-lung epithelial cells.