ArticleJournal of cellular and molecular medicine2008
Spliceosomal protein E regulates neoplastic cell growth by modulating expression of cyclin E/CDK2 and G2/M checkpoint proteins.
Article in Journal of cellular and molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- RETRACTION: Spliceosomal Protein E Regulates Neoplastic Cell Growth by Modulating Expression of Cyclin E/CDK2 and G2/M Checkpoint Proteins.Journal of cellular and molecular medicine · 2026Article
- SNRPB promotes gastric cancer progression by regulating aberrant splicing of PUF60.Cell death & disease · 2025Article
- SNRPE is Associated with ERK/mTOR Signaling Activation and Reduced Autophagy to Promote Lung Adenocarcinoma Cell Proliferation.OncoTargets and therapy · 2025Article
- Oncofetal SNRPE promotes HCC tumorigenesis by regulating the FGFR4 expression through alternative splicing.British journal of cancer · 2024Article
- Therapy-induced secretion of spliceosomal components mediates pro-survival crosstalk between ovarian cancer cells.Nature communications · 2024Article
- [Regulatory effect of small nuclear ribonucleoprotein-associated protein B on proliferation and metastasis of liver cancer cells].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022Article
- ORN: Inferring patient-specific dysregulation status of pathway modules in cancer with OR-gate Network.PLoS computational biology · 2021Article
- Quantitative proteomic analysis of the association between decreasing O‑GlcNAcylation and metastasis in MCF‑7 breast cancer cells.International journal of oncology · 2020Article
- SNRPB promotes the tumorigenic potential of NSCLC in part by regulating RAB26.Cell death & disease · 2019Article
- Divaricoside Exerts Antitumor Effects, in Part, by Modulating Mcl-1 in Human Oral Squamous Cell Carcinoma Cells.Computational and structural biotechnology journal · 2019Article
- Therapy-induced stress response is associated with downregulation of pre-mRNA splicing in cancer cells.Genome medicine · 2018Article
- A Flavone Constituent from Myoporum bontioides Induces M-Phase Cell Cycle Arrest of MCF-7 Breast Cancer Cells.Molecules (Basel, Switzerland) · 2017Article
- Graded requirement for the spliceosome in cell cycle progression.Cell cycle (Georgetown, Tex.) · 2015Article
- Overexpression of DOC-1R inhibits cell cycle G1/S transition by repressing CDK2 expression and activation.International journal of biological sciences · 2013Article
- Identification of novel deregulated RNA metabolism-related genes in non-small cell lung cancer.PloS one · 2012Article
- Alternative splicing and tumor progression.Current genomics · 2008Article
- The ruthenium(II)-arene compound RAPTA-C induces apoptosis in EAC cells through mitochondrial and p53-JNK pathways.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2008Article
- Effects of excretory/secretory products from Clonorchis sinensis and the carcinogen dimethylnitrosamine on the proliferation and cell cycle modulation of human epithelial HEK293T cells.The Korean journal of parasitology · 2008Article
Corrections and comments
- Retracted
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small nuclear ribonucleoproteins are essential splicing factors. We previously identified the spliceosomal protein E (SmE) as a downstream effector of E2F1 in p53-deficient human carcinoma cells. Here, we investigated the biological relevance of SmE in determining the fate of cancer and non-tumourigenic cells. Adenovirus-mediated expression of SmE selectively reduces growth of cancerous cells due to decreased cell proliferation but not apoptosis. A similar growth inhibitory effect for SmD1 suggests that this is a general function of Sm-family members. Deletion of Sm-motifs reveals the importance of the Sm-1 domain for growth suppression. Consistently, SmE overexpression leads to inhibition of DNA synthesis and G2 arrest as shown by BrdU-incorporation and MPM2-staining. Real-time RT-PCR and immunoblotting showed that growth arrest by SmE directly correlates with the reduction of cyclin E, CDK2, CDC25C and CDC2 expression, and up-regulation of p27Kip. Importantly, SmE activity was not associated with enhanced expression of other spliceosome components such as U1 SnRNP70, suggesting that the growth inhibitory effect of SmE is distinct from its pre-mRNA splicing function. Furthermore, specific inactivation of SmE by shRNA significantly increased the percentage of cells in S phase, whereas the amount of G2/M arrested cells was reduced. Our data provide evidence that Sm proteins function as suppressors of tumour cell growth and may have major implications as cancer therapeutics.
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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.