Human papillomavirus E6 and E7 oncogenes (HPV E6/E7)

Human papillomavirus (HPV) E6 and E7 are the primary oncogenes responsible for the development of HPV-associated malignancies, including cervical, oropharyngeal, and anal cancers [1, 2]. These genes are constitutively expressed in infected cells and are essential for the maintenance of the malignant phenotype [3, 5]. The E6 protein primarily functions by inducing the ubiquitin-mediated degradation of the tumor suppressor p53, thereby preventing apoptosis and allowing the survival of cells with DNA damage [2, 4]. Simultaneously, the E7 protein binds to and inactivates the retinoblastoma protein (pRb), which releases E2F transcription factors and drives the cell into the S-phase of the cell cycle [2, 11]. Because these viral genes are absent in healthy human cells, they serve as highly specific targets for therapeutic intervention [5, 7]. Current therapeutic approaches include DNA vaccines like VGX-3100, which deliver synthetic E6 and E7 DNA to stimulate a T-cell-mediated immune response against infected cells [5, 10]. Emerging technologies such as CRISPR/Cas9 and RNA interference are also being explored to directly disrupt the viral DNA or silence the resulting mRNA transcripts [7, 17, 18]. These targeted therapies aim to restore host tumor suppressor functions and induce apoptosis specifically in cancerous cells [5, 17].

Other names

HPV16 E6/E7HPV18 E6/E7Human papillomavirus early genes E6 and E7HPV E6 and E7 oncogene DNAHPV E6/E7 genes

Therapeutic DNA vaccination to induce T-cell mediated immunity; Gene silencing via CRISPR/Cas9 or RNA interference; Transcriptional inhibition of viral early promoters.