Anti-WNT7A monoclonal antibody Made to order

Oral squamous cell carcinoma (OSCC) is the most common type and most threatening head and neck cancer worldwide. Here, we aim to study the relationship between the WNT7A-beta-Catenin signaling pathway and the chemotherapy resistance of OSCC patients. We analyzed 42 OSCC patients and 19 adjacent non-tumor tissues, evaluated the expression levels of WNT7A mRNA, and subsequently studied WNT7A dependent cisplatin resistance in OSCC cell line KB cells. Moreover, we also utilized an in vivo mouse model to validate our findings. We first found a significant upregulation of WNT7A mRNA in OSCC patients. Our results showed that the knockdown of WNT7A sensitized KB cells to cisplatin. Moreover, our results revealed that nuclear beta-catenin was dramatically reduced and cleaved caspase-3 and cleaved PARP were dramatically induced when WNT7A was knocked down in cisplatin treated KB cells. Besides, we found that the knockdown of WNT7A significantly reduced the weight and volumes of xenograft tumors. Moreover, we examined apoptotic cells and found that the combination of WNT7A knockdown and cisplatin treatment resulted in many more apoptotic cells than cisplatin treatment alone, suggesting that the knockdown of WNT7A sensitized KB cells to cisplatin treatment in vivo. Our results revealed that inhibition of WNT7A-beta-catenin signaling sensitizes OSCC to cisplatin, which has provided insights into the molecular diagnosis and treatment of OSCC.

Retinal pigment epithelium (RPE) cell damage underlies many degenerative, dystrophic, and proliferative diseases of the human retina. Primary adult human RPE cells can be used for in vitro modeling of RPE cell behavior under pathological conditions. We demonstrated previously that Wnt7. inhibits adult human RPE cell proliferation, and initiates the spread and polarization of dedifferentiated RPE cells on a plastic surface. Here, we investigated the role of Wnt7a in the regulation of RPE cell plasticity, at cellular and molecular levels. Protein expression and localization were examined by immunofluorescence analysis, while mRNA expression was quantified by real-time PCR. The obtained results showed that Wnt7. influences the expression of a range of neural differentiation markers (nestin, MAP1B, beta-tubulin III, synapsin I, 200 kDa and 68 kDa neurofilaments), and increases the expression of various RPE differentiation markers (RPE65, MITF, OTX2, and Pax6). Our findings indicate that Wnt7a exerts a pleiotropic effect on RPE cells in vitro, stimulating redifferentiation (RPE properties), while maintaining neural differentiation indicators. Although this effect was shown to be reversible, Wnt7a may act as a regulator of RPE cell plasticity, and may represent a potential therapeutic target for the prevention of RPE transformation.