TY - JOUR
T1 - Overexpression of genes involved in miRNA biogenesis in medullary thyroid carcinomas with RET mutation
AU - Puppin, Cinzia
AU - Durante, Cosimo
AU - Sponziello, Marialuisa
AU - Verrienti, Antonella
AU - Pecce, Valeria
AU - Lavarone, Elisa
AU - Baldan, Federica
AU - Campese, Antonio Francesco
AU - Boichard, Amelie
AU - Lacroix, Ludovic
AU - Russo, Diego
AU - Filetti, Sebastiano
AU - Damante, Giuseppe
N1 - Publisher Copyright:
© 2014, Springer Science+Business Media New York.
PY - 2014/10/21
Y1 - 2014/10/21
N2 - Abnormal expression of non-coding micro RNA (miRNA) has been described in medullary thyroid carcinoma (MTC). Expression of genes encoding factors involved in miRNA biogenesis results often deregulated in human cancer and correlates with aggressive clinical behavior. In this study, expression of four genes involved in miRNA biogenesis (DICER, DROSHA, DCGR8, and XPO5) was investigated in 54 specimens of MTC. Among them, 33 and 13 harbored RET and RAS mutations, respectively. DICER, DGCR8, and XPO5 mRNA levels were significantly overexpressed in MTC harboring RET mutations, in particular, in the presence of RET634 mutation. When MTCs with RET and RAS mutations were compared, only DGCR8 displayed a significant difference, while MTCs with RAS mutations did not show significant differences with respect to non-mutated tumors. We then attempted to correlate expression of miRNA biogenesis genes with tumor aggressiveness. According to the TNM status, MTCs were divided in two groups and compared (N0 M0 vs. N1 and/or M1): for all four genes no significant difference was detected. Cell line experiments, in which expression of a RET mutation is silenced by siRNA, suggest the existence of a causal relationship between RET mutation and overexpression of DICER, DGCR8, and XPO5 genes. These findings demonstrate that RET- but not RAS-driven tumorigenic alterations include abnormalities in the expression of some important genes involved in miRNA biogenesis that could represent new potential markers for targeted therapies in the treatment of RET-mutated MTCs aimed to restore the normal miRNA expression profile.
AB - Abnormal expression of non-coding micro RNA (miRNA) has been described in medullary thyroid carcinoma (MTC). Expression of genes encoding factors involved in miRNA biogenesis results often deregulated in human cancer and correlates with aggressive clinical behavior. In this study, expression of four genes involved in miRNA biogenesis (DICER, DROSHA, DCGR8, and XPO5) was investigated in 54 specimens of MTC. Among them, 33 and 13 harbored RET and RAS mutations, respectively. DICER, DGCR8, and XPO5 mRNA levels were significantly overexpressed in MTC harboring RET mutations, in particular, in the presence of RET634 mutation. When MTCs with RET and RAS mutations were compared, only DGCR8 displayed a significant difference, while MTCs with RAS mutations did not show significant differences with respect to non-mutated tumors. We then attempted to correlate expression of miRNA biogenesis genes with tumor aggressiveness. According to the TNM status, MTCs were divided in two groups and compared (N0 M0 vs. N1 and/or M1): for all four genes no significant difference was detected. Cell line experiments, in which expression of a RET mutation is silenced by siRNA, suggest the existence of a causal relationship between RET mutation and overexpression of DICER, DGCR8, and XPO5 genes. These findings demonstrate that RET- but not RAS-driven tumorigenic alterations include abnormalities in the expression of some important genes involved in miRNA biogenesis that could represent new potential markers for targeted therapies in the treatment of RET-mutated MTCs aimed to restore the normal miRNA expression profile.
KW - DGCR8
KW - DICER
KW - Medullary thyroid carcinoma
KW - XPO5
KW - miRNA
UR - http://www.scopus.com/inward/record.url?scp=84911003417&partnerID=8YFLogxK
U2 - 10.1007/s12020-014-0204-3
DO - 10.1007/s12020-014-0204-3
M3 - Article
C2 - 24569963
AN - SCOPUS:84911003417
SN - 1355-008X
VL - 47
SP - 528
EP - 536
JO - Endocrine
JF - Endocrine
IS - 2
ER -