Lymphoma is the most common malignant
tumor arising from immune system. Recently,
DNA polymerase epsilon subunit 2 (POLE2) was identified to be a
tumor promotor in a variety of malignant
tumors. However, the
biological role of POLE2 in
lymphoma is still largely unclear. In our present study, the expression patterns of POLE2 in
lymphoma tissues were identified by immunohistochemistry (IHC) staining of human tissue microarray. Cell viability was determined by
CCK-8 assay. Cell apoptosis and cycle distribution were evaluated by
Annexin V and PI staining, respectively. Cell migration was analyzed by transwell assay.
Tumor growth in vivo was observed by a xenograft model of mice. The potential signaling was explored by human phospho-
kinase array and immunoblotting. POLE2 was significantly upregulated in human
lymphoma tissues and cells. POLE2 knockdown attenuated the proliferation, migration capabilities of
lymphoma cells, as well as induced cell apoptosis and cycle arrest. Moreover, POLE2 depletion impaired the
tumor growth in mice. Furthermore, POLE2 knockdown apparently inhibited the activation of β-
Catenin and downregulated the expression of Wnt/β-
Catenin signaling-related
proteins. POLE2 knockdown suppressed the proliferation and migration of
lymphoma cells by inhibiting Wnt/β-
Catenin signaling pathway. POLE2 may serve as a novel therapeutic target for
lymphoma.