Anti-WNT10B monoclonal antibody, clone 6B8

Epithelial-mesenchymal transition (EMT) plays a critical role in the process of cancer invasion and metastasis. The Wnt/beta-catenin signaling pathway is known as a stimulative factor, which may trigger EMT and metastasis of cancer cells. In addition, several microRNAs (miRNAs) have been proven to regulate the EMT process. Recent research revealed that miR-148a is downregulated in pancreatic cancer. However, the definite role of miR-148a in EMT and invasion of pancreatic cancer is still unknown. The present study attempted to demonstrate the underlying mechanism of miR-148a in the regulation of EMT and invasion of pancreatic cancer cells. Our data revealed that the expression of miR-148a was markedly downregulated in human pancreatic ductal adenocarcinoma (PDAC) cell lines and tissues. In addition, the downregulation of miR-148a was associated with poor prognosis and EMT phenotype. Furthermore, restoration of miR-148a expression inhibited the EMT process, as well as the migration and invasion of BxPC-3 pancreatic cancer cells. Wnt10b, a promoting molecule of the Wnt/beta-catenin signaling pathway, was demonstrated by dual-luciferase reporter assay to be a direct target of miR-148a. Subsequently, we found that miR-148a negatively regulated the protein expression of beta-catenin, cyclin D1 and MMP-9, which were important components of the Wnt/beta-catenin signaling pathway. In conclusion, these findings revealed that miR-148a suppresses EMT and invasion of pancreatic cancer cells by targeting Wnt10b and inhibiting the Wnt/beta-catenin signaling pathway, and thus, miR-148a may serve as a novel therapeutic target for pancreatic cancer.

Hair loss is characterized by a shortened hair anagen phase and hair follicles (HF) miniaturization. Morroniside is the most abundant iridoid glycoside extracted from Cornus officinalis and has various bioactivities in different cell functions and tissue regeneration. In this study, we investigated the effects and the underlying mechanism of morroniside on hair growth and regulation of HF cycle transition. Morroniside treatment significantly enhanced outer root sheath cell (ORSC) proliferation and migration in vitro. Additionally, morroniside upregulated Wnt10b, beta-catenin and lef1. The enhanced ORSC proliferation and migration due to morroniside treatment were partly rescued by a Wnt/beta-catenin signaling inhibitor, DKK1. Furthermore, in a hair-induced mouse model, morroniside injection accelerated the onset of anagen and delayed HF catagen, as shown by histological examination. Immunohistochemical analyses revealed that Wnt/beta-catenin signaling pathway expression was upregulated in the HFs. These findings suggest that morroniside regulates HF growth and development partly through the Wnt/beta-catenin signaling pathway and may be a potential treatment for hair loss.