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Molecular interactions of ‘high risk’ human papillomaviruses E6 and E7 oncoproteins: implications for tumour progression

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Abstract

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 thatE6 andE7 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.

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Abbreviations

Ad:

Adenovirus

AP:

associated protein

APC:

adenomatous polyposis coli

CBP:

CREB binding protein

CIN:

cervical intraepithelial neoplasia

HDAC:

histone deacetylases

HPVs:

human papillomaviruses

hTERT:

human telomerase catalytic subunit

ICC:

invasive cervical carcinoma

IGFBP-3:

insulin-like growth factor binding protein-3

IRF-3:

interferon regulatory factor-3

M2-PK:

M2 pyruvate kinase

Rb:

retinoblastoma

TAF-110:

TBP-associated factor-110

TGF:

transforming growth factor

TNF-α:

tumour necrosis factor-α

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Correspondence to Oishee Chakrabarti.

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Chakrabarti, O., Krishna, S. Molecular interactions of ‘high risk’ human papillomaviruses E6 and E7 oncoproteins: implications for tumour progression. J. Biosci. 28, 337–348 (2003). https://doi.org/10.1007/BF02970152

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