作者: Andreia Bufalino , Nilva K. Cervigne , Carine Ervolino de Oliveira , Felipe Paiva Fonseca , Priscila Campioni Rodrigues
DOI: 10.1371/JOURNAL.PONE.0136599
关键词:
摘要: Deregulated expression of activin A is reported in several tumors, but its biological functions oral squamous cell carcinoma (OSCC) are unknown. Here, we investigate whether can play a causal role OSCCs. Activin was assessed by qPCR and immunohistochemistry OSCC tissues. Low A-expressing cells were treated with recombinant for apoptosis, proliferation, adhesion, migration, invasion epithelial-mesenchymal transition (EMT). Those phenotypes also evaluated high follistatin (an antagonist) or stably expressing shRNA targeting A. Transfections microRNA mimics performed to determine the overexpression regulated miR-143/miR-145 cluster. overexpressed OSCCs comparison normal mucosa, levels significantly associated lymph node metastasis, tumor differentiation poor survival. High promoted multiple properties malignant transformation, including decreased apoptosis increased EMT. Both miR-143 miR-145 markedly downregulated lines clinical specimens, inversely correlated levels. Forced Overexpression OSCCs, which controlled downregulation cluster, regulates proliferation invasiveness, it clinically metastasis