RETRACTED: MicroRNA-140 Inhibits the Epithelial-Mesenchymal Transition and Metastasis in Colorectal Cancer
Author(s) -
Jiazhi Li,
Kun Zou,
Lihui Yu,
Wenyue Zhao,
Ying Lü,
Jun Mao,
Bo Wang,
Lu Wang,
Shujun Fan,
Bo Song,
Lianhong Li
Publication year - 2018
Publication title -
molecular therapy — nucleic acids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.208
H-Index - 59
ISSN - 2162-2531
DOI - 10.1016/j.omtn.2017.12.022
Subject(s) - epithelial–mesenchymal transition , colorectal cancer , metastasis , microrna , cancer research , cancer metastasis , cancer , medicine , oncology , biology , gene , genetics
MicroRNA-140, a cartilage-specific microRNA, has recently been implicated in the cancer progression. However, the comprehensive role of miR-140 in the invasion and metastasis of colorectal cancer (CRC) is still not fully understood. In this study, we confirmed that miR-140 downregulates SMAD family member 3 (Smad3), which is a key downstream effector of the TGF-β signaling pathway, at the translational level in the CRC cell lines. Ectopic expression of miR-140 inhibits the process of epithelial-mesenchymal transition (EMT), at least partially through targeting Smad3, and induces the suppression of migratory and invasive capacities of CRC cells in vitro. miR-140 also attenuates CRC cell proliferation possibly via downregulating Samd3. Furthermore, overexpression of miR-140 inhibits the tumor formation and metastasis of CRC in vivo, and silenced Smad3 has the similar effect. Additionally, miR-140 expression is decreased in the clinical primary CRC specimens and appears as a progressive reduction in the metastatic specimens, whereas Smad3 is overexpressed in the CRC samples. Taken together, our findings suggest that miR-140 might be a key suppressor of CRC progression and metastasis through inhibiting EMT process by targeting Smad3. miR-140 may represent a novel candidate for CRC treatment.
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