construct in these 4 NSCLC cell lines. We discovered a high c-MYC
reporter activity in the cell lines with high hPAF1 protein level
(A549 and H838), low activity of the c-MYC reporter in H1650 cells
with low hPAF1 protein level, and almost no detectable c-MYC reporter
activity in the H2170 cells (Fig. 3B). Thus, the fact that the
expression of one hPAF1C factor is close correlated with that of cMYC
at both RNA and protein levels strongly suggests that hPAF1C
play an active role in c-MYC transcriptional activity.
To investigate the effects of hPAF1C inhibition, we utilized
hPAF1etargeted siRNAs to knock-down the protein level of hPAF1.
The transfection of siRNA was conducted according to standard
protocol and the knock-down efficiency was evaluated through
western blot analysis. Interestingly, we found that the treatment of
hPAF1 siRNA also resulted in obvious reduction of c-MYC expression
(Fig. 3C). These results highlight a positive correlation between
endogenous hPAF1 and c-MYC expressions in NSCLC samples, and
the reduction of hPAF1 expression also down-regulate the
expression of c-MYC in NSCLC cells.