| Summary: | Merkel cell polyomavirus (MCV) is the first polyomavirus that can cause human
cancer, and was discovered in January of 2008 (Huichen Feng, 2008). Its large T
antigen shares structural and sequential similarities with SV40 T antigen and
functional similarities with Human Papillomavirus (HPV) E7 proteins. These viral
proteins have tumor transforming ability by binding to the tumor suppressor protein
Retinoblastoma (Rb). In HPV infected cells, E7 binds to Rb and disrupts the Rb-E2F
complex. Accumulation of free E2F then induces p16 expression (Samir N. Khleif, et
al. 1996). Our hypothesis was if MCV and SV40 T antigens use the same
mechanism, we should be able to observe induced p16 expression in cells
transfected with MCV and SV40 T antigen plasmids. The p16 expression in LNCap
cells transfected with SV40 and MCV full-length and C-terminal truncated T antigen
plasmids were detected by immunofluorescence and western blot. Increased p16
expression was only observed in MCV full-length T antigen but not in truncated MCV
T antigen or SV40 T antigen transfected cells. The results might be associated with
different effects of epigenetic modification by MCV and SV40 T antigens.
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