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Merck
CN
  • SENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expression.

SENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expression.

Cell death discovery (2021-07-28)
Yali Zhang, Yanni Ma, Guixian Wu, Mingling Xie, Chengxin Luo, Xiangtao Huang, Feng Tian, Jieping Chen, Xi Li
摘要

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.

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Roche
原位细胞死亡检测试剂盒,TMR红, sufficient for ≤50 tests