Expression of far upstream element binding protein 1 in B‑cell non‑Hodgkin lymphoma is correlated with tumor growth and cell‑adhesion mediated drug resistance.

Cell adhesion-mediated drug resistance (CAM-DR) remains a major obstacle to the effectiveness of chemotherapeutic treatment of lymphoma. Far upstream element binding protein 1 (FBP1) is a multifunctional protein that is highly expressed in proliferating cells of several solid neoplasms; however, its expression and biological function in B-cell lymphoma is largely unknown. FBP1 expression in both reactive lymphoid tissues and several B-cell lymphomas, including follicular lymphoma and diffuse large B-cell lymphoma were detected by immunohistochemistry analysis. FBP1 expression in B-cell lymphoma was also associated with poor survival outcomes. Functionally, small interfering RNA-mediated silencing of FBP1 was able to inhibit the proliferation of B-cell lymphoma cells, resulting in G(0)/G(1) phase cell cycle arrest. Furthermore, results of a cell adhesion assay demonstrated that adhesion to fibronectin or bone marrow stromal cells induced FBP1 expression, which in turn facilitated cell adhesion. Finally, FBP1 knockdown reversed CAM-DR. These findings support a role for FBP1 in non-Hodgkin lymphoma cell proliferation, adhesion and drug resistance, and may lead to the generation of a novel therapeutic approach targeting this molecule.