TY - JOUR
T1 - MiR-21 coordinates tumor growth and modulates KRIT1 levels
AU - Orso, Francesca
AU - Balzac, Fiorella
AU - Marino, Marco
AU - Lembo, Antonio
AU - Retta, Saverio Francesco
AU - Taverna, Daniela
N1 - Funding Information:
We thank L. Xu, R. Hynes and L. Primo for providing cell lines, D. Corà for helping with initial bioinformatics, V. Monica and L. Goitre for participating to the preparation of some tools. Grant support: This work was supported by Grants from the University of Torino (Local Research Funding 2007/DT, 2008/D. T. , 2007/SFR, 2008/S. F. R. ), Compagnia di San Paolo (D.T.), Torino , PRIN 2008 (D.T.), AIRC 2010 ( IG 10104 D. T. ), FIRB giovani ( RBFR08F2FS-002 F. O. ), PRIN 2008 ( 2008BP25KN to S.F.R.) and Fondazione Telethon ( GGP06222 to S.F.R.).
PY - 2013/8/16
Y1 - 2013/8/16
N2 - miR-21 is overexpressed in tumors and it displays oncogenic activity. Here, we show that expression of miR-21 in primary tumors anticorrelates with KRIT1/CCM1, an interacting partner of the Ras-like GTPase Rap1, involved in Cerebral Cavernous Malformations (CCM). We present evidences that miR-21 silences KRIT1 by targeting its mRNA 3'UTR and that this interaction is involved in tumor growth control. In fact, miR-21 over-expression or KRIT1 knock-down promote anchorage independent tumor cell growth compared to controls, whereas the opposite is observed when anti-miR-21 or KRIT1 overexpression are employed. Our findings suggest that miR-21 promotes tumor cell growth, at least in part, by down-modulating the potential tumor suppressor KRIT1.
AB - miR-21 is overexpressed in tumors and it displays oncogenic activity. Here, we show that expression of miR-21 in primary tumors anticorrelates with KRIT1/CCM1, an interacting partner of the Ras-like GTPase Rap1, involved in Cerebral Cavernous Malformations (CCM). We present evidences that miR-21 silences KRIT1 by targeting its mRNA 3'UTR and that this interaction is involved in tumor growth control. In fact, miR-21 over-expression or KRIT1 knock-down promote anchorage independent tumor cell growth compared to controls, whereas the opposite is observed when anti-miR-21 or KRIT1 overexpression are employed. Our findings suggest that miR-21 promotes tumor cell growth, at least in part, by down-modulating the potential tumor suppressor KRIT1.
KW - KRIT1
KW - MiR-21
KW - Tumor growth
UR - https://www.scopus.com/pages/publications/84881551605
U2 - 10.1016/j.bbrc.2013.07.031
DO - 10.1016/j.bbrc.2013.07.031
M3 - Article
SN - 0006-291X
VL - 438
SP - 90
EP - 96
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -