The expression of c-MYC suggests downregulation of BCL-2 and may open the road to use of anti-Topoisomerases.
The danger of c-MYC is through its relation with ZBTB17(Zinc Finger) which affects the Host Cell Factor 1 which in turn hits SP1 and the POU2F1. The latest activates:
"POU2F1 has been shown to interact with SNAPC4,[3][4] Ku80,[5][6] Glucocorticoid receptor,[7][8][9] Sp1 transcription factor,[10][11] NPAT,[12] POU2AF1,[4][13][14] Host cell factor C1,[15][16] TATA binding protein,[17] RELA,[18] Nuclear receptor co-repressor 2,[19] EPRS,[20] Glyceraldehyde 3-phosphate dehydrogenase,[12] MNAT1[21] and Retinoid X receptor alpha.[7][22]"wikipedia
Touching the RELA in an uncontrolled fashon is generally a mistake. It is a "wilder" gene affecting all functions and marks the Wnt/NFkB involvement, and Brings in the Casein Kinases.
The involvement of PPP1R13L further brings in the SP-1, amplifying downstream events.
Amplification of the c-MYC could always be associated with repression of Myb which impacts the mi-RNA 155, and may be associated with explosive expression of the c-FOS that needs Tamper! Of course presence of c-FOS will lead to more AP-1, should c-JUN be present! Increase of c-FOS could raise the importance of Histone de-acetylators in this disease!
So the presence of c-FOS and c-MYC could potentially raise the importance of Etoposide and Histone deacetylators! An interesting trial to suggest....
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