Human Papillomavirus Type 16 E6 and E7 Cause Polyploidy in Human Keratinocytes and Up-Regulation of G2-M-phase Proteins

Daksha Patel; A. Incassati; N. Wang; Dennis McCance

doi:10.1158/0008-5472.CAN-03-2917

Human Papillomavirus Type 16 E6 and E7 Cause Polyploidy in Human Keratinocytes and Up-Regulation of G2-M-phase Proteins

Daksha Patel, A. Incassati, N. Wang, Dennis McCance

Research output: Contribution to journal › Article › peer-review

79 Citations (Scopus)

Abstract

Human papillomavirus type 16 proteins E6 and E7 have been shown to cause centrosome amplification and lagging chromosomes during mitosis. These abnormalities during mitosis can result in missegregation of the chromosomes, leading to chromosomal instability. Genomic instability is thought to be an essential part of the conversion of a normal cell to a cancer cell. We now show that E6 and E7 together cause polyploidy in primary human keratinocytes soon after these genes are introduced into the cells. Polyploidy seems to result from a spindle checkpoint failure arising from abrogation of the normal functions of p53 and retinoblastoma family members by E6 and E7, respectively. In addition, E6 and E7 cause deregulation of cellular genes such as Plk1, Aurora-A, cdk1, and Nek2, which are known to control the G2-M-phase transition and the ordered progression through mitosis.

Original language	English
Pages (from-to)	1299-1306
Number of pages	8
Journal	Cancer Research
Volume	64(4)
Issue number	4
DOIs	https://doi.org/10.1158/0008-5472.CAN-03-2917
Publication status	Published - 15 Feb 2004

ASJC Scopus subject areas

Cancer Research
Oncology

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1158/0008-5472.CAN-03-2917

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title = "Human Papillomavirus Type 16 E6 and E7 Cause Polyploidy in Human Keratinocytes and Up-Regulation of G2-M-phase Proteins",

abstract = "Human papillomavirus type 16 proteins E6 and E7 have been shown to cause centrosome amplification and lagging chromosomes during mitosis. These abnormalities during mitosis can result in missegregation of the chromosomes, leading to chromosomal instability. Genomic instability is thought to be an essential part of the conversion of a normal cell to a cancer cell. We now show that E6 and E7 together cause polyploidy in primary human keratinocytes soon after these genes are introduced into the cells. Polyploidy seems to result from a spindle checkpoint failure arising from abrogation of the normal functions of p53 and retinoblastoma family members by E6 and E7, respectively. In addition, E6 and E7 cause deregulation of cellular genes such as Plk1, Aurora-A, cdk1, and Nek2, which are known to control the G2-M-phase transition and the ordered progression through mitosis.",

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AU - Incassati, A.

AU - Wang, N.

AU - McCance, Dennis

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Human Papillomavirus Type 16 E6 and E7 Cause Polyploidy in Human Keratinocytes and Up-Regulation of G2-M-phase Proteins

Abstract

ASJC Scopus subject areas

UN SDGs

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