SOCS2 and neoplasm: Taken together, we found SENP1 was upregulated in MCL patients and cell lines; knockdown of SENP1 inhibited MCL cell proliferation and promoted cell apoptosis, and also inhibited MCL tumor growth in mice; knockdown of SENP1 resulted in inhibition of JAK-STAT5 pathway and increased the expression of tumor suppressor SOCS2.