SENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expression
Abstract 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...
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| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Nature Publishing Group
2021-07-01
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| Series: | Cell Death Discovery |
| Online Access: | https://doi.org/10.1038/s41420-021-00578-x |
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| _version_ | 1849726778941112320 |
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| author | Yali Zhang Yanni Ma Guixian Wu Mingling Xie Chengxin Luo Xiangtao Huang Feng Tian Jieping Chen Xi Li |
| author_facet | Yali Zhang Yanni Ma Guixian Wu Mingling Xie Chengxin Luo Xiangtao Huang Feng Tian Jieping Chen Xi Li |
| author_sort | Yali Zhang |
| collection | DOAJ |
| description | Abstract 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. |
| format | Article |
| id | doaj-art-979a48d7da584b8d910f71830feffd07 |
| institution | DOAJ |
| issn | 2058-7716 |
| language | English |
| publishDate | 2021-07-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Cell Death Discovery |
| spelling | doaj-art-979a48d7da584b8d910f71830feffd072025-08-20T03:10:05ZengNature Publishing GroupCell Death Discovery2058-77162021-07-017111010.1038/s41420-021-00578-xSENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expressionYali Zhang0Yanni Ma1Guixian Wu2Mingling Xie3Chengxin Luo4Xiangtao Huang5Feng Tian6Jieping Chen7Xi Li8Department of Hematology, Southwest Hospital, Army Medical University (Third Military Medical University)Department of Hematology, Southwest Hospital, Army Medical University (Third Military Medical University)Department of Hematology, Southwest Hospital, Army Medical University (Third Military Medical University)Department of Hematology, Southwest Hospital, Army Medical University (Third Military Medical University)Department of Hematology, Southwest Hospital, Army Medical University (Third Military Medical University)Department of Hematology, Southwest Hospital, Army Medical University (Third Military Medical University)Department of Hepatobiliary Surgery, Southwest Hospital, Army Medical University (Third Military Medical University)Department of Hematology, Southwest Hospital, Army Medical University (Third Military Medical University)Department of Hematology, Southwest Hospital, Army Medical University (Third Military Medical University)Abstract 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.https://doi.org/10.1038/s41420-021-00578-x |
| spellingShingle | Yali Zhang Yanni Ma Guixian Wu Mingling Xie Chengxin Luo Xiangtao Huang Feng Tian Jieping Chen Xi Li SENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expression Cell Death Discovery |
| title | SENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expression |
| title_full | SENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expression |
| title_fullStr | SENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expression |
| title_full_unstemmed | SENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expression |
| title_short | SENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expression |
| title_sort | senp1 promotes mcl pathogenesis through regulating jak stat5 pathway and socs2 expression |
| url | https://doi.org/10.1038/s41420-021-00578-x |
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