KSHV and HPV modulate epithelial-to-mesenchymal transition in oral epithelial cells.

ABSTRACT: Most oral viral infections that manifest as oral diseases or cancers are caused by oncogenic human papillomavirus and herpesviruses. However, the mechanisms involved in the association between oral cancer and oncogenic virus infection are not well understood. In this study, we used telomerase (hTERT) -immortalized normal oral gingival keratinocytes (NOKs) and generated latent Kaposi's sarcoma-associated herpesvirus (KSHV)- and human papillomavirus 31 (HPV31)-infected NOKs. NOKs either stably maintaining HPV episomes or latently infected with KSHV acquired a fibroblast-like morphology and upregulated cell proliferation in both complete media and serum starvation culture conditions. Moreover, migration and invasion assays revealed that the KSHV- and HPV-infected NOKs show markedly higher mig

SUBMITTER: Li Q 

PROVIDER: S-EPMC12421897 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature