Human papillomaviruses (HPVs) are known to utilize the
down-regulation of epithelial (E)-cadherin, a major component
of adherens junctions of keratinocytes, to evade host
immune surveillance in high-risk group. However, the effects
of HPV on the function of E-cadherin in low-risk groups remain
unknown. We investigated whether type 2 HPV (HPV-
2) E7 could induce alterations in E-cadherin expression in
transiently transfected keratinocytes and cell lines expressing
HPV-2 E7. To examine the expression pattern of E-cadherin
in cutaneous warts and normal skin samples, immunohistochemical
analysis was performed. Quantitative real-time
polymerase chain reactions, luciferase assays, western blot,
immunocytochemistry, and electron microscopy were used
to evaluate the mRNA and protein expression levels of Ecadherin
in normal human epidermal keratinocytes transfected
with HPV-2 E7 plasmid DNA or E7-specific siRNA
and in E7-expressing cell lines. E-cadherin expression levels
in HPV-2 positive cutaneous warts were significantly decreased
compared to those in normal skin (p < 0.05). Similarly,
the mRNA and protein expression levels of E-cadherin
in E7 transiently transfected cells were significantly decreased
compared to those in empty vector-transfected cells. The decreases
were restored by transfection with E7-specific siRNA
(p < 0.05). Likewise, cell lines expressing E7 showed a decreased
expression of E-cadherin. When the cells were cultured
in low attachment plates, cell-to-cell aggregation was
inhibited. Taken together, our data suggest that HPV-2 E7,
the causative agent of cutaneous warts, could mediate the
transcriptional repression of E-cadherin.
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