@mastersthesis{10902/26006,
year = {2022},
month = {6},
url = {https://hdl.handle.net/10902/26006},
abstract = {ABSTRACT :
MYC oncoprotein belongs to a protein-interaction network that include proteins of the MXD 
family, as both MYC and MXD proteins have a common interaction partner: MAX. MYC is deregulated 
in up to 60% of human tumors and has a crucial role in the initiation and progression of cancer. 
Unfortunately, MYC has proven to be a difficult therapeutic target. For this reason, the study of the 
MYC network proteins is important. The most relevant MXD proteins is MNT, because it is ubiquitously 
expressed and is deregulated in tumors. MNT is labelled as tumor suppressor being an antagonist of 
MYC, but in some models it cooperates with MYC promoting cell proliferation and survival. Our lab 
has previously demonstrated a MNT-CCDC6 interaction. CCDC6 is a protein involved in DNA damage 
repair and a tumor suppressor. Thus, I have studied the activity of MNT and CCDC6 as they can provide 
the basis for alternative strategies to impair MYC activity in cancer. One of the tumors showing frequent 
MNT deregulation or deletions is cutaneous T cell lymphoma (CTCL) and thus we focused in CTCL 
cell lines. First, using Western Blot, I have compared MNT and CCDC6 expression in several human 
lymphoma cells. Then I have performed co-immunoprecipitation experiments to investigate the MNT CCD6 interaction in the cell lines with significant expression of both genes. I have also silenced MNT 
with short-hairpin methodology, using lentiviral vectors to analyze the effect of MNT depletion on 
proliferation of the lymphoma cells. Silencing was confirmed by western blot. An increase of 
proliferation was detected in at least once cell line.},
title = {MNT and CCDC6 in cutaneous T cell  lymphoma cells},
author = {Saidi, Khouloud},
}