Critical role of miR-10b in transforming growth factor-β1-induced epithelial-mesenchymal transition in breast cancer.
Epithelial-mesenchymal transition (EMT) is a key process in the tumor metastatic cascade that is characterized by the loss of cell-cell junctions and cell polarity, resulting in the acquisition of migratory and invasive properties. Recent evidence showed that altered microRNA-10b (miR-10b) expression was implicated in the occurrence of EMT of breast cancer. However, the exact role and underlying mechanisms of miR-10b in the EMT of breast cancer still remain unknown. In this study, miR-10b was found to be upregulated in breast cancer tissues and breast cancer cell lines and the expression of miR-10b was shown to be closely correlated with aggressiveness in breast cancer. Treating breast cancer cells with the miR-10b inhibitor increased E-cadherin expression while decreasing vimentin expression. At the same time, on inhibition of miR-10b, the invasion and proliferation ability of breast cancer cells also decreased. Transforming growth factor-β (TGF-β) is a multifunctional cytokine that induces EMT in multiple cell types. Here, we identified miR-10b as a target gene of TGF-β1. The expression of miR-10b increased during TGF-β1-induced EMT of breast cancer cells. Further study showed that inhibition of miR-10b expression partially reversed the EMT, invasion and proliferation induced by TGF-β1 in breast cancer cells. Taken together, these results demonstrated a novel function for miR-10b in TGF-β1-induced EMT in breast cancer and increased their metastatic potential. MiR-10b might become a possible target for gene therapy in breast cancer.
Department of Breast Disease Surgery, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Xu
X
Han
Department of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Sun
S
Yan
Department of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Zhang
Z
Weijie
Department of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Wang
W
Feng
Department of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Wang
W
Liuxing
Department of Breast Disease Surgery, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Li
L
Mengquan
Department of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Fan
F
Qingxia
D000704:Analysis of Variance; D015153:Blotting, Western; D001943:Breast Neoplasms / Q000235:genetics* / Q000503:physiopathology*; D015820:Cadherins / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D018076:DNA, Complementary / Q000096:biosynthesis; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics / Q000502:physiology*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D035683:MicroRNAs / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009361:Neoplasm Invasiveness / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D053773:Transforming Growth Factor beta1 / Q000378:metabolism / Q000494:pharmacology*; D014746:Vimentin / Q000378:metabolism
D015820:Cadherins; D018076:DNA, Complementary; C547183:MIRN10 microRNA, human; D035683:MicroRNAs; C508960:TGFB1 protein, human; D053773:Transforming Growth Factor beta1; D014746:Vimentin