I am reading the following paper: Development and characterization of an enhanced nonviral
expression vector for electroporation cancer treatment - Patrick F Forde1, Lindsay J Hall2, Mira Sadadcharam1, Marcle de Kruijf1, Gerald C O’ Sullivan1 and Declan M Soden.
what they say is that: " our construction of pEEV, we utilized components of the SFV, and we therefore hypothesized that the nonviral pEEV may delay tumor growth due to excessive gene expression inducing oncolytic activity and leading to cell lysis of transfected cells" ......
AND
" This approach was also found to have several advantages specifically for cancer therapy including: greatly improved and consistent gene
expression and eventual direct oncolytic effect (cellular exhaustion) from continued mRNA production, which obviates the risk of long term
exogenous gene expression.
i am confused, what is causing the oncolytic activity, i thought that viruses normally cause membrane breakdown therefore cell lysis. but they say its because of excessive gene expression by the self amplifying plasmid, which causes cell exhaustion causing the cell lysis. So how does this work? i thought cancer cells were always excessively expressing genes because they continuosly dividing so they sholdnt become exhauseted? or have i assumed wrong
. please guide me !
thank you
-KhaleesiDany-
The presence of the "p" in pEEV and the non-viral vector are the hints here - this is a plasmid not a virus.
-bob1-
bob1 on Sat Aug 30 23:53:59 2014 said:
The presence of the "p" in pEEV and the non-viral vector are the hints here - this is a plasmid not a virus.
i get that. but they say because they utilized viral components, they tested for oncolytic activity. so i am asking how excessive gene expression causes oncolytic activity. in cancer cells that are ever growing is there no excessive gene expression already? im not sure what exactly happens in cancer cells hence the confusion
-KhaleesiDany-
The components might be very stong promoters, which would induce continuous high gene expression independent of the cell cycle.
-bob1-
