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. 2024 Feb;44(1):134-143.
doi: 10.1007/s11596-024-2829-7. Epub 2024 Jan 25.

SENP3 Promotes Mantle Cell Lymphoma Development through Regulating Wnt10a Expression

Affiliations

SENP3 Promotes Mantle Cell Lymphoma Development through Regulating Wnt10a Expression

Yan-Ni Ma et al. Curr Med Sci. 2024 Feb.

Abstract

Objective: SUMO-specific protease 3 (SENP3), a member of the SUMO-specific protease family, reverses the SUMOylation of SUMO-2/3 conjugates. Dysregulation of SENP3 has been proven to be involved in the development of various tumors. However, its role in mantle cell lymphoma (MCL), a highly aggressive lymphoma, remains unclear. This study was aimed to elucidate the effect of SENP3 in MCL.

Methods: The expression of SENP3 in MCL cells and tissue samples was detected by RT-qPCR, Western blotting or immunohistochemistry. MCL cells with stable SENP3 knockdown were constructed using short hairpin RNAs. Cell proliferation was assessed by CCK-8 assay, and cell apoptosis was determined by flow cytometry. mRNA sequencing (mRNA-seq) was used to investigate the underlying mechanism of SENP3 knockdown on MCL development. A xenograft nude mouse model was established to evaluate the effect of SENP3 on MCL growth in vivo.

Results: SENP3 was upregulated in MCL patient samples and cells. Knockdown of SENP3 in MCL cells inhibited cell proliferation and promoted cell apoptosis. Meanwhile, the canonical Wnt signaling pathway and the expression of Wnt10a were suppressed after SENP3 knockdown. Furthermore, the growth of MCL cells in vivo was significantly inhibited after SENP3 knockdown in a xenograft nude mouse model.

Conclusion: SENP3 participants in the development of MCL and may serve as a therapeutic target for MCL.

Keywords: SENP3; apoptosis; cell proliferation; mantle cell lymphoma.

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References

    1. Wilson MR, Barrett A, Cheah CY, et al. How I manage mantle cell lymphoma: indolent versus aggressive disease. Br J Haematol, 2023,201(2):185–198 - DOI - PubMed
    1. Kumar A, Sha F, Toure A, et al. Patterns of survival in patients with recurrent mantle cell lymphoma in the modern era: progressive shortening in response duration and survival after each relapse. Blood Cancer J, 2019,9(6):50 - DOI - PubMed - PMC
    1. Jain P, Wang M. Mantle cell lymphoma: 2019 update on the diagnosis, pathogenesis, prognostication, and management. Am J Hematol, 2019,94(6):710–725 - DOI - PubMed
    1. Zhang Y, Ma Y, Wu G, et al. SENP1 promotes MCL pathogenesis through regulating JAK-STAT5 pathway and SOCS2 expression. Cell Death Discov, 2021,7(1):192 - DOI - PubMed - PMC
    1. Fernàndez V, Hartmann E, Ott G, et al. Pathogenesis of mantle-cell lymphoma: all oncogenic roads lead to dysregulation of cell cycle and DNA damage response pathways. J Clin Oncol, 2005,23(26):6364–6369 - DOI - PubMed

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