Molecular Signature of HPV-Induced Carcinogenesis: pRb, p53 and Gene Expression Profiling

摘要: The infection by mucosal human papillomavirus (HPV) is causally associated with tumor development in cervix and oropharynx. mechanisms responsible for this oncogenic potential are mainly due to the product activities of two early viral oncogenes: E6 E7. Although a large number cellular targets have been described both oncoproteins, interaction suppressors p53 retinoblastoma protein (pRb) emerged as key functional activities. degrades suppressor p53, thus inhibiting p53-dependent functions, whereas E7 binds pRb, allowing transcription E2F-dependent genes. Since these exert their actions through transcriptional modulation, genomics has provided body data that reflects altered gene expression HPVinfected cells or tissues. Here we will review similarities differences findings, also compare them those obtained transgenic mouse models bearing deletion some oncogene targets. comparative analysis supports molecular evidences about role oncogenes interference mentioned suggests mice can be used HPV-associated diseases such cervical, oropharynx, skin carcinomas.