Mantle cell lymphoma (MCL) is highly aggressive and its treatment remains challenging, understanding its pathogenesis is critical for future targeted therapy. SUMO specific proteases 1 (SENP1) is an important protein that regulates the balance between SUMOylation and deSUMOylation. We found that SENP1 was upregulated in MCL patient samples and cell lines. Knockdown of SENP1 could inhibit the proliferation and promote the apoptosis of MCL cells. We also found that SENP1 knockdown caused inhibition of the JAK-STAT5 pathway and upregulation of tumor suppressor cytokine signaling 2 (SOCS2). Moreover, MCL tumor growth in vivo was significantly suppressed after SENP1 knockdown in a xenograft nude mouse model. In summary, our results showed that SENP1 is involved in the pathogenesis of MCL and may be a potential therapeutic target.

套细胞淋巴瘤（MCL）具有高度侵袭性，其治疗仍然具有挑战性，了解其发病机制对于未来的靶向治疗至关重要。SUMO 特异性蛋白酶 1 (SENP1) 是调节 SUMO 化和去 SUMO 化之间平衡的重要蛋白质。我们发现 SENP1 在 MCL 患者样本和细胞系中表达上调。敲低SENP1可以抑制MCL细胞的增殖并促进其凋亡。我们还发现 SENP1 敲低导致 JAK-STAT5 通路受到抑制，肿瘤抑制细胞因子信号传导 2 (SOCS2) 上调。此外，在异种移植裸鼠模型中，SENP1敲除后，体内MCL肿瘤的生长受到显着抑制。总之，我们的结果表明SENP1参与了MCL的发病机制，并可能是一个潜在的治疗靶点。