High Expression of CIP2A Can Promote the Proliferation, Migration, and Epithelial-Mesenchymal Transition of Diffuse Large B-Cell Lymphoma Cells.

Abstract

Diffuse large B-cell lymphoma (DLBC) is one of the usual forms found in indolent or invasive non-Hodgkin's lymphoma. Cancerous inhibitor of protein phosphatase 2A (CIP2A) has been revealed to be dysregulated in multiple cancers and is closely associated with tumor growth. However, the regulatory influences of CIP2A in DLBC progression remain unclear. The protein expressions were determined through western blot. Cell survival was assessed through the CCK-8 assay. Cell proliferation was examined through colony formation assay. The cell migration and invasion were inspected through transwell assay. First, it was discovered that CIP2A exhibited higher expression in DLBC. Additionally, inhibition of CIP2A restrained cell growth and metastasis in DLBC. Next, it was discovered that E-cadherin protein expression was ascended as well as N-cadherin and α-SMA protein expressions were descended after CIP2A knockdown, indicating that CIP2A suppression can retard the epithelial-mesenchymal transition (EMT) progress in DLBC. Finally, it was demonstrated that suppression of CIP2A retarded the Wnt/β-catenin pathway. It was manifested that high expression of CIP2A can aggrandize cell proliferation, migration, and EMT process in DLBC, and triggered the Wnt/β-catenin pathway. This finding implied that CIP2A may serve as a hopeful target for treating DLBC.