SENP1 (SUMO Specific Peptidase 1)

HBx-SENP1's role in regulating CSC-associated properties was examined in vitro (stemness expression, sphere formation, CD133+ cells, migration/invasion, and sorafenib sensitivity) and in vivo using an orthotopic xenograft model...Findings from this research highlight that HBx-induced SENP1 is crucial for promoting CSC-associated properties in HCC. SENP1 could serve as a novel biomarker of early tumor recurrence and metastasis, especially for HBV-related HCC.

Complementary enrichment and immune-infiltration analyses link higher SENP1 expression to tumor-promoting pathways, upregulation of immune-checkpoint genes (PD-L1, PD-1, CTLA4), and reduced microsatellite instability, suggesting a role in immune evasion. Collectively, these findings identify SENP1 as a prognostic marker and potential therapeutic target in GC, with putative involvement in both tumor progression and modulation of the tumor immune microenvironment.

Previous studies have shown that Cfz is associated with a higher incidence of severe adverse cardiac effects than bortezomib (Btz); however, the underlying mechanisms remain to be elucidated. Therefore, the overexpression of SENP1 using AAV vectors alleviates Cfz-induced cardiotoxicity in mice. In summary, our findings reveal a previously unknown role of the SENP1-DDX17 axis in protecting against cardiotoxicity induced by Cfz, providing a potential foundation for developing therapeutic strategies to mitigate cardiac side effects in the clinical management of MM patients.

Originally, a concentration of 2 μg/ml dacarbazine (DTIC) was employed in the treatment of A375 and M14 cell lines for a duration of 24 h. Subsequently, the cells were transferred to fresh medium and allowed to proliferate until reaching 80% of their maximum density...This study suggests that there is a positive correlation between the ubiquitin-specific protease SENP1 and drug resistance in melanoma. Its up-regulation may lead to changes in the deSUMOylation of YAP, activate the Hippo signalling pathway, and increase the resistance of melanoma to DTIC.

The involvement of SENP1 represents a pivotal role in governing the nucleocytoplasmic shuttling of p27kip1. SENP1 knockdown could effectively impede CCA cell proliferation and enhance the chemosensitivity of cis‑platinum by modulating the nuclear export of p27kip1 through SUMOylation, thus offering a potential therapeutic approach for CCA in the future.

The prognostic and immunogenetic value of SENP1 and SENP5 in HCC was demonstrated in this study. Therefore, these two genes have the potential to function as separate prognostic biomarkers and offer promise as immunotherapeutic targets in the fight against HCC.

This study explores the molecular mechanism by which sentrin/SUMO-specific protease 1 (SENP1) promotes cisplatin (Cis) resistance and tumor stem cell characteristics in colon adenocarcinoma (COAD) through desumoylation-mediated modification of octamer-binding transcription factor 4 (OCT4)...In vivo, SENP1 knockdown reduced tumor growth and stem cell markers, while OCT4 overexpression escalated tumor metastasis and structural damage. These findings demonstrate that SENP1's modulation of OCT4 is central to COAD's resistance and stem cell properties, offering a novel target for COAD therapy.

Moreover, the expression levels of SENP1 and YBX1 were both increased in CRC specimens and associated with poor outcomes in CRC patients. In general, our studies have revealed SENP1-mediated YBX1 protein deSUMOylation promotes CRC progression through the activation of AKT phosphorylation signaling, suggesting that targeting the SENP1-YBX1-AKT signaling axis is a promising therapeutic strategy for CRC.

Also, a negative correlation between hnRNPM SUMOylation and SENP1 expression or phosphorylated PFKFB3 levels can be found in CRC patient samples. These findings not only enhance our understanding of the multifaceted roles of hnRNPM in cancer biology but also open new avenues for the development of targeted therapies aimed at modulating hnRNPM SUMOylation.

This article provides a review of the latest research on HAPC in various omics techniques, hematopoietic regulation and diagnostic processes which is more conducive to understand the pathogenesis. The clinical diagnosis of excessive erythrocytosis emphasizes the importance of genetic testing.

YBX1 is a KMT2D-mediated H3K4me1-binding effector protein and mutation of YBX1 (E121A) disrupts its binding to H3K4me1. KMT2D and YBX1 cooperatively promote TNBC proliferation and metastasis by activating c-Myc and SENP1 expression in vitro and in vivo. YBX1 is colocalized with H3K4me1 in the c-Myc and SENP1 promoter regions in TNBC cells and increased YBX1 expression predicts a poor prognosis in breast cancer patients.

Our findings reveal a distinct mechanism of SENP1-mediated HDAC2-AKT activation and establish the critical role of the IGF2BP3/SENP1signaling axis in AML development.