Molecular interactions of 'high risk' human papillomaviruses E6 and E7 oncoproteins: implications for tumour progression.
The aetiology of cervical cancer has been primarily attributed to human papillomaviruses (HPVs). These are characterized by the persistent expression of the two oncogenes, E6 and E7. Experimental studies show that E6 and E7 genes of the high risk HPVs deregulate key cell cycle controls. Recent work has uncovered new cellular partners for these proteins that throw light on many of the pathways and processes in which these viral proteins intervene. This review focuses on the regulation of host proteins by the viral oncoproteins and consequence of such interactions on cell survival, proliferation, differentiation and apoptosis.
National Centre for Biological Sciences, Tata Institute of Fundamental Research, UAS-GKVK Campus, Bangalore 560 065, India. oishee@ncbs.res.in
Oishee
O
Chakrabarti
Sudhir
S
Krishna
D017209:Apoptosis; D002455:Cell Division; D002472:Cell Transformation, Viral; D018450:Disease Progression; D005260:Female; D015967:Gene Expression Regulation, Viral; D006801:Humans; D009856:Oncogene Proteins, Viral / Q000235:genetics / Q000378:metabolism*; D027383:Papillomaviridae / Q000235:genetics / Q000378:metabolism*; D050725:Papillomavirus E7 Proteins; D030361:Papillomavirus Infections / Q000473:pathology / Q000821:virology*; D012097:Repressor Proteins; D012307:Risk Factors; D014158:Transcription, Genetic; D002583:Uterine Cervical Neoplasms / Q000473:pathology / Q000821:virology*
C068651:E6 protein, Human papillomavirus type 16; D009856:Oncogene Proteins, Viral; D050725:Papillomavirus E7 Proteins; D012097:Repressor Proteins; C059731:oncogene protein E7, Human papillomavirus type 16