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Last update 08 May 2025

SND1

Last update 08 May 2025

Basic Info

Synonyms

100 kDa coactivator, EBNA2 coactivator p100, p100

+ [6]

Introduction

Endonuclease that mediates miRNA decay of both protein-free and AGO2-loaded miRNAs (PubMed:18453631, PubMed:28546213). As part of its function in miRNA decay, regulates mRNAs involved in G1-to-S phase transition (PubMed:28546213). Functions as a bridging factor between STAT6 and the basal transcription factor (PubMed:12234934). Plays a role in PIM1 regulation of MYB activity (PubMed:9809063). Functions as a transcriptional coactivator for STAT5 (By similarity). (Microbial infection) Promotes SARS-CoV-2 RNA synthesis by binding to negative-sense RNA and the viral protein nsp9. (Microbial infection) Functions as a transcriptional coactivator for the Epstein-Barr virus nuclear antigen 2 (EBNA2).

Drugs associated with SND1

MTDH/SND1 inhibitors(China Pharmaceutical University)

Target

MTDH x SND1

Mechanism

MTDH inhibitors [+1]

Active Org.

China Pharmaceutical University

Originator Org.

China Pharmaceutical University

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SND1

100 Translational Medicine associated with SND1

0 Patents (Medical) associated with SND1

251

Literatures (Medical) associated with SND1

03 Feb 2025·Journal of Clinical Investigation

Translational regulation of SND1 governs endothelial homeostasis during stress

Article

Author: Ong, Sang-Ging ; Baranov, Pavel V ; Han, Zhenbo ; Tahmasebi, Soroush ; Zhang, Sen ; Tabatabaei, Negar ; Kiniry, Stephen ; Pinho, Sandra ; Amiri, Mehdi ; Rehman, Jalees ; Kwon, Youjeong ; Nukala, Sarath Babu ; Ong, Sang-Bing ; Yan, Gege ; Jousma, Jordan

Translational control shapes the proteome and is particularly important in regulating gene expression under stress. A key source of endothelial stress is treatment with tyrosine kinase inhibitors (TKIs), which lowers cancer mortality but increases cardiovascular mortality. Using a human induced pluripotent stem cell-derived endothelial cell (hiPSC-EC) model of sunitinib-induced vascular dysfunction combined with ribosome profiling, we assessed the role of translational control in hiPSC-ECs in response to stress. We identified staphylococcal nuclease and tudor domain-containing protein 1 (SND1) as a sunitinib-dependent translationally repressed gene. SND1 translational repression was mediated by the mTORC1/4E-BP1 pathway. SND1 inhibition led to endothelial dysfunction, whereas SND1 OE protected against sunitinib-induced endothelial dysfunction. Mechanistically, SND1 transcriptionally regulated UBE2N, an E2-conjugating enzyme that mediates K63-linked ubiquitination. UBE2N along with the E3 ligases RNF8 and RNF168 regulated the DNA damage repair response pathway to mitigate the deleterious effects of sunitinib. In silico analysis of FDA-approved drugs led to the identification of an ACE inhibitor, ramipril, that protected against sunitinib-induced vascular dysfunction in vitro and in vivo, all while preserving the efficacy of cancer therapy. Our study established a central role for translational control of SND1 in sunitinib-induced endothelial dysfunction that could potentially be therapeutically targeted to reduce sunitinib-induced vascular toxicity.

01 Feb 2025·Pathology - Research and Practice

Whole genome and transcriptome analysis of pancreatic acinar cell carcinoma elucidates mechanisms of homologous recombination deficiency and unravels novel relevant fusion events

Article

Author: Deshpande, Aditya ; Delgado-de la Mora, Jesús ; Sigouros, Michael ; Halima, Ahmed ; Lieberman, Michael D ; Hadi, Kevin ; Manohar, Jyothi ; Ocean, Allyson J ; Mosquera, Juan Miguel ; Popa, Elizabeta C ; Al Assaad, Majd ; Medina-Martínez, Juan S ; Karaaslan, Selda ; Sboner, Andrea ; Elemento, Olivier ; Hissong, Erika ; Jessurun, José

Pancreatic acinar cell carcinoma (PACC) is a rare pancreatic tumor with a heterogeneous clinical course and, except for radical surgery, limited treatment options. We present a comprehensive study encompassing whole-genome and RNA sequencing of 7 tumor samples from 3 metastatic PACC patients to further delineate its genomic landscape and potential therapeutic implications. Our findings reveal distinct signatures of homologous recombination deficiency (HRD) in patients harboring pathogenic germline BRCA1/2 and FANCL mutations, demonstrating favorable responses to poly (ADP-ribose) polymerase 1 (PARP) inhibitors with prolonged disease-free intervals. Additionally, we first describe structural variants in PACC, including BRCA1::TRIM47 fusion and another variant impacting FANCC, both events related to HRD, and we also identify alterations in the mitogen-activated protein kinase (MAPK) pathway, including RAF1 duplication as well as novel BRAF::SORBS2 and MAP7D2::SND1 gene fusions, offering potential targets for therapy. Our study underscores the importance of genome and transcriptome-wide profiling of PACC, to help guide personalized treatment strategies to improve patient outcomes.

01 Feb 2025·International Journal of Biological Macromolecules

SND1–SMARCA5 interaction strengthened by PIM promotes the proliferation, metastasis, and chemoresistance of esophageal squamous cell carcinoma

Article

Author: Han, Fei ; Han, Bin ; Tang, XiaoPing ; Long, Yang ; Yin, Hui ; Zhou, Min ; Gao, Yan ; Wang, Chao ; Xu, Tao ; Hu, Zhi ; Huang, Shan ; Yan, QunLun ; Li, Yuan ; Dai, TianYang ; Wu, Jian ; Deng, Xin

Chromatin remodeling plays a pivotal role in the progression of esophageal squamous cell carcinoma (ESCC), but the precise mechanisms remain poorly understood. Here, we elucidated the critical function of staphylococcal nuclease and tudor domain-containing 1 (SND1) in modulating chromatin dynamics, thereby driving ESCC progression in both in vitro and in vivo models. Our data revealed that SND1 was markedly overexpressed in ESCC cell lines. Silencing SND1 disrupted histone modifications, attenuated RNA polymerase II activity, and precipitated increased chromosomal aberrations and DNA damage, particularly following camptothecin treatment. These molecular perturbations culminated in diminished cellular proliferation, metastasis, and chemoresistance. We further identified that the regulatory effects of SND1 on chromatin were mediated through its interaction with SMARCA5, a process potentiated by PIM1-catalyzed phosphorylation of SND1 at serine 426. This SND1-SMARCA5 interaction was essential for the transcriptional activation of CUX1, a key oncogene implicated in ESCC progression. Notably, disruption of SND1^S426 phosphorylation impaired the SND1-SMARCA5 interaction, leading to significant inhibition of ESCC tumor growth and metastatic potential in vivo. Our findings unveil a novel mechanistic axis involving SND1 and SMARCA5 in chromatin remodeling and oncogenesis, offering promising therapeutic targets for ESCC intervention.

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SND1

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