Differential expression of p53 and p21 in low grade cervical squamous intraepithelial lesions infected with low, intermediate, and high risk human papillomaviruses

Alphavirus M1 induces apoptosis of malignant glioma cells via downregulation and nucleolar translocation of p21WAF1/CIP1 protein

“…For example, downregulation of p21 by E6 of HPV-16, a causative factor in cervical cancer, was shown to play a key role in apoptosis. 16,20 Thus, the possibility of a unifying mechanism underlying apoptosis induced by these different viruses is very intriguing to us.…”

“…[16][17][18][19] Notably, downregulation of p21 was shown to be important for apoptosis induced by virus, 16,20 UV-irradiation 21,22 or chemotherapy agent. 23 However, the role played by cell cycle regulators (for example, p21, CDK2 and cyclin D) in alphavirus-induced apoptosis is largely unknown.…”

The Indicators of Predicting Disease Outcome in HPV Carcinogenesis

“…The loss of cell-cycle control by HPV oncoproteins directly or indirectly interacting with the host genes (Giannoudis et al, 2000) leads to accelerated proliferation mirrored by an increased number of cells expressing specific markers. Among cyclins and cyclin dependent kinases (CDKs) that governed cell cycle, p53, Rb and CDK inhibitors (p15, p16, p18, p19, p21, p27) play a special role by arresting the cell cycle until damaged DNA is completely repaired.…”

Genomic Instability Induced By Human Papillomavirus Oncogenes

“…10 Polyploidy can lead to both numerical and structural chromosome abnormalities by increasing the rate of DNA breakage and damage,11,12 the latter has been shown to be an anti-cancer barrier in early human tumorigenesis.13,14 Tetrasomy in basal keratinocytes has been found in low-grade squamous intra-epithelial lesions of the cervix infected with highrisk but not low-risk HPV types. 15 Significantly, a recent study demonstrated that tetraploidy occurred as an early event during cervical carcinogenesis and predisposed cells to aneuploidy. 16 Two other recent studies demonstrated that tetraploid but not diploid mouse or human cells are competent to induce tumors with both numerical and structural chromosome abnormalities.…”