A microRNA code for prostate cancer metastasis

被引：107

作者：

Bonci, D. ^{[1
,2
]}

Coppola, V. ^{[1
]}

Patrizii, M. ^{[1
]}

Addario, A. ^{[1
]}

Cannistraci, A. ^{[1
]}

Francescangeli, F. ^{[1
]}

Pecci, R. ^{[3
]}

Muto, G. ^{[4
,5
]}

Collura, D. ^{[4
]}

Bedini, R. ^{[3
]}

Zeuner, A. ^{[1
]}

Valtieri, M. ^{[1
]}

Sentinelli, S. ^{[2
]}

Benassi, M. S. ^{[6
]}

Gallucci, M. ^{[2
]}

Carlini, P. ^{[2
]}

Piccolo, S. ^{[7
]}

De Maria, R. ^{[2
]}

机构：

[1] Ist Super Sanita, Dept Hematol Oncol & Mol Med, Viale Regina Elena 299, I-00161 Rome, Italy

[2] Regina Elena Inst Canc Res, Sci Directorate, Rome, Italy

[3] Ist Super Sanita, Dept Technol & Hlth, Viale Regina Elena 299, I-00161 Rome, Italy

[4] S Giovanni Bosco Hosp, Dept Urol, Turin, Italy

[5] Campus Biomed Univ, Dept Urol, Rome, Italy

[6] Ist Ortoped Rizzoli, Lab Expt Oncol, Bologna, Italy

[7] Univ Padua, Sch Med, Dept Mol Med, Padua, Italy

来源：

ONCOGENE | 2016年 / 35卷 / 09期

关键词：

EPITHELIAL-MESENCHYMAL TRANSITION; GROWTH-FACTOR-BETA; TGF-BETA; BREAST-CANCER; STEM-CELLS; BONE-METASTASIS; SELF-RENEWAL; TUMOR; RAS; PROGRESSION;

D O I：

10.1038/onc.2015.176

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Although the development of bone metastasis is a major detrimental event in prostate cancer, the molecular mechanisms responsible for bone homing and destruction remain largely unknown. Here we show that loss of miR-15 and miR-16 in cooperation with increased miR-21 expression promote prostate cancer spreading and bone lesions. This combination of microRNA endows bone-metastatic potential to prostate cancer cells. Concomitant loss of miR-15/miR-16 and gain of miR-21 aberrantly activate TGF-beta and Hedgehog signaling, that mediate local invasion, distant bone marrow colonization and osteolysis by prostate cancer cells. These findings establish a new molecular circuitry for prostate cancer metastasis that was validated in patients' cohorts. Our data indicate a network of biomarkers and druggable pathways to improve patient treatment.

引用

页码：1180 / 1192

页数：13

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