ArticleOncogene2014
The transcriptional co-activator SND1 is a novel regulator of alternative splicing in prostate cancer cells.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 82 citations in OpenAlex.
- Molecular Pathophysiology of Hepatocellular Carcinoma: From Metabolic Inflammation to Therapeutic Targets.Cancers · 2026Review
- Lipidation as a post-translational code for protein liquid-liquid phase separation.Journal of lipid research · 2026Review
- Staphylococcal nuclease and tudor domain-containing protein 1: An emerging therapeutic target in cancer (Review).Molecular and clinical oncology · 2025Review
- Breaking the oncogenic alliance: advances in disrupting the MTDH-SND1 complex for cancer therapy.RSC advances · 2025Review
- The Valsa mali Effector VmSR1 Accelerates the Degradation of Tudor-SN2 to Suppress RNA Silencing and Plant Immunity.Molecular plant pathology · 2025Article
- The crosstalk between SND1 and PDCD4 is associated with chemoresistance of non-small cell lung carcinoma cells.Cell death discovery · 2025Article
- A novel partnership between lncTCF7 and SND1 regulates the expression of the TCF7 gene via recruitment of the SWI/SNF complex.Scientific reports · 2024Article
- Loss of the methylarginine reader function of SND1 confers resistance to hepatocellular carcinoma.The Biochemical journal · 2023Article
- SND1 binds to ERG and promotes tumor growth in genetic mouse models of prostate cancer.Nature communications · 2023Article
- The RNA-binding protein Snd1/Tudor-SN regulates hypoxia-responsive gene expression.FASEB bioAdvances · 2023Article
- Effectors and effects of arginine methylation.Biochemical Society transactions · 2023Article
- RNA-binding proteins regulating the CD44 alternative splicing.Frontiers in molecular biosciences · 2023Review
- Inhibition of SND1 overcomes chemoresistance in bladder cancer cells by promoting ferroptosis.Oncology reports · 2023Article
- DNA Damage Regulates the Functions of the RNA Binding Protein Sam68 through ATM-Dependent Phosphorylation.Cancers · 2022Article
- Inhibition of RNA Binding in SND1 Increases the Levels of miR-1-3p and Sensitizes Cancer Cells to Navitoclax.Cancers · 2022Article
- Abrogation of HnRNP L enhances anti-PD-1 therapy efficacyActa pharmaceutica Sinica. B · 2022Article
- Functional Interaction Between the Oncogenic Kinase NEK2 and Sam68 Promotes a Splicing Program Involved in Migration and Invasion in Triple-Negative Breast Cancer.Frontiers in oncology · 2022Article
- Mitochondrion-Localized SND1 Promotes Mitophagy and Liver Cancer Progression Through PGAM5.Frontiers in oncology · 2022Article
- SPT6 recruits SND1 to co-activate human telomerase reverse transcriptase to promote colon cancer progression.Molecular oncology · 2021Article
- PAX5 activates telomerase activity and proliferation in keloid fibroblasts by transcriptional regulation of SND1, thus promoting keloid growth in burn-injured skin.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Splicing abnormalities have profound impact in human cancer. Several splicing factors, including SAM68, have pro-oncogenic functions, and their increased expression often correlates with human cancer development and progression. Herein, we have identified using mass spectrometry proteins that interact with endogenous SAM68 in prostate cancer (PCa) cells. Among other interesting proteins, we have characterized the interaction of SAM68 with SND1, a transcriptional co-activator that binds spliceosome components, thus coupling transcription and splicing. We found that both SAM68 and SND1 are upregulated in PCa cells with respect to benign prostate cells. Upregulation of SND1 exerts a synergic effect with SAM68 on exon v5 inclusion in the CD44 mRNA. The effect of SND1 on CD44 splicing required SAM68, as it was compromised after knockdown of this protein or mutation of the SAM68-binding sites in the CD44 pre-mRNA. More generally, we found that SND1 promotes the inclusion of CD44 variable exons by recruiting SAM68 and spliceosomal components on CD44 pre-mRNA. Inclusion of the variable exons in CD44 correlates with increased proliferation, motility and invasiveness of cancer cells. Strikingly, we found that knockdown of SND1, or SAM68, reduced proliferation and migration of PCa cells. Thus, our findings strongly suggest that SND1 is a novel regulator of alternative splicing that promotes PCa cell growth and survival.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.