Anti-YAP1 (internal region) polyclonal antibody

Background: Osteoporosis is a systemic bone disease resulting from decreased bone mass and bone microstructure degeneration. Yes-associated protein 1 (YAP1) belongs to YAP family and plays a significant part in controlling bone quality. Aim of the study: Present study aimed to study the function and up-stream mechanism of YAP1 in the differentiation of BMSCs (bone marrow stromal cells) and MC3T3-E1. Methods: ALP staining, alizarin red staining and western blot analysis of osteogenic biomarkers determined osteogenic differentiation in BMSCs and MC3T3-E1. Mechanistic assays including luciferase reporter assay, RIP assay and RNA pull down assay disclosed the interplays between RNAs. Results: YAP1 promoted osteogenic differentiation of BMSCs and MC3T3-E1. Circ_0024097 originated from YAP1 sponged miR-376b-3p to elevate YAP1 expression in BMSCs and MC3T3-E1. Further, YAP1 mediated circ_0024097- promoted effects on osteogenic differentiation. Moreover, circ_0024097 activated Wnt/beta-catenin pathway to facilitate osteogenic differentiation. Conclusion: It was firstly uncovered in present study that circ_0024097 attenuated osteoporosis through promoting osteogenic differentiation via miR-376b-3p/YAP1 axis and Wnt/beta-catenin pathway.

Hepatocellular carcinoma is one of the most common gastrointestinal malignancies. Anti-angiogenesis therapies have recently demonstrated promise in the treatment of malignancies, although early treatment benefits may be accompanied by metastasis over time. Additional and more effective anti-angiogenic treatment modalities are therefore needed. We previously found that Yes-associated protein 1 (YAP1) expression is increased in hepatocellular carcinoma (HCC), particularly around tumor-associated blood vessels, suggesting a role in angiogenesis. The YAP1 inhibitor verteporfin is presently in anti-angiogenic clinical trials for the treatment of various cancers. Depleted YAP1 from vascular endothelial cells effectively reduced proliferation and tube formation, validating its utility as an anti-angiogenesis target. We also showed that YAP1 depletion or inhibition in vascular endothelial cells leads to increased release of exosomes containing the long non-coding RNA (lncRNA) MALAT1 into the tumor microenvironment. Direct exosomal transfer of MALAT1 to hepatic cells leads to increased hepatic cell invasion and migration via activation of extracellular signal-regulated kinase 1/2 (ERK1/2) signaling. These observations may explain the occurrence of distant tumor metastasis with YAP1-associated anti-angiogenic therapy over time. It provides insight into new pathways and treatment paradigms that may be targeted to increase the long-term success of anti-angiogenic therapies.