Unit:
Τομέας Βιολογίας Κυττάρου Και ΒιοφυσικήςLibrary of the School of Science
Author:
Θανασοπούλου Αγγελική
Dissertation committee:
Ι. Παπασιδέρη Αναπλ. Καθηγ.(Επιβλέπουσα), Λ. Μαργαρίτης Ομ. Καθηγ. Δ. Στραβοπόδης Επικ. Καθηγ.
Original Title:
Μελέτη του κυτταροβιολογικού ρόλου της πρωτεΐνης H4/CCDC6 σε πρότυπα βιολογικά συστήματα
Summary:
CCDC6 gene, (also known as H4, D10S170 or PTC1) encodes a conserved and
ubiquitously expressed protein. It was first isolated and identified due to its
participation to the paracentric inversion inv(10)(q11.2q210) which is found in
the 25% of cases of papillary thyroid carcinoma. It also participates in the
formation of the fusion gene H4/PDGFRβ, which is a product of chromosomal
translocation (5;10)(q33;q22) and is present in sporadic cases of chronic
myeloid leukemia.
The main goal of this thesis was to clarify the physiological role of Ccdc6, to
further characterize the effect of loss of Ccdc6 normal function on cellular
processes and whether this effect can contribute to cancer formation. Taken
together, with the fulfillment of this thesis we were able to place CCDC6
regulatory protein in the master cellular signaling pathway of the cell cycle
and genome preservation and to propose new proteins (14-3-3σ, CDC25C, p53 and
Lamin-Β) that interact with CCDC6 and create new networks for the cellular
physiology. Finally, our findings strongly suggested that deregulation of Ccdc6
impaired the ability of the cell to maintain genomic integrity and created a
prosperous ground for genomic instability and cancer formation. A specific
mechanism for this was proposed. This knowledge offers a better understanding
of the molecular events that lead to cancer development and hence could unravel
new molecular approaches for targeting the malignancies where CCDC6 is altered.
Keywords:
cancer, papillary thyroid carcinoma, chronic myeloid leukemia, cell cycle, genomic instability
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