Journal
MOLECULAR PHARMACOLOGY
Volume 95, Issue 4, Pages 451-461Publisher
AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
DOI: 10.1124/mol.118.114207
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Funding
- National Natural Science Foundation of China [81830078, 81772347, 81572123]
- Science and Technology Commission of Shanghai Municipality [16430723500]
- Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant Support [20161314]
- Shanghai Shen Kang hospital development center [16CR2036B]
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Several microRNAs (miRNAs) have been found expressed differentially in osteosarcoma (OS), so they may function in the onset and progression of OS. In this study, we found that miR-144 significantly suppresses osteosarcoma cell proliferation, migration, and invasion ability in vitro and inhibited tumor growth and metastasis in vivo. Mechanically, we demonstrated that Ras homolog family member A (RhoA) and its pivotal downstream effector Rho-associated, coiled-coil-containing protein kinase 1 (ROCK1) were direct targets of miR-144. Moreover, the negative correlation between down-regulated nniR-144 and up-regulated ROCK1/RhoA was verified in both OS cell lines and clinical patients' specimens. Functionally, RhoA with or without ROCK1 co-overexpression resulted a rescue phenotype on miR-144 inhibited cell growth, migration, and invasion abilities whereas individual overexpression of ROCK1 had no statistical significance compared with controls in nniR-144-transfected SAOS2 and U2-OS cells. Taken together, this study demonstrates that miR-144 inhibited tumor growth and metastasis OS via dual-suppressing of RhoA and ROCK1, which could be a new therapeutic approach for the treatment of OS.
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