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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 G0/G1 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.

molecular medicine reports

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