ArticleBMC cell biology2004
Sam68 exerts separable effects on cell cycle progression and apoptosis.
Article in BMC cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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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Who cites it
38 citing papers in PubMed, 101 citations in OpenAlex.
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- Cdk1-mediated threonine phosphorylation of Sam68 modulates its RNA binding, alternative splicing activity and cellular functions.Nucleic acids research · 2022Article
- Role of Sam68 in Sunitinib induced renal cell carcinoma apoptosis.Cancer medicine · 2022Article
- Structure, Function, and Regulation of the SRMS Tyrosine Kinase.International journal of molecular sciences · 2020Review
- Leptin, Adiponectin, and Sam68 in Bone Metastasis from Breast Cancer.International journal of molecular sciences · 2020Review
- Sam68 mediates high glucose‑induced podocyte apoptosis through modulation of Bax/Bcl‑2.Molecular medicine reports · 2019Article
- Apoptosis and Autophagy in Picornavirus Infection.Frontiers in microbiology · 2019Review
- Review
- High expression of Sam68 in sacral chordomas is associated with worse clinical outcomes.OncoTargets and therapy · 2017Article
- The p53 status can influence the role of Sam68 in tumorigenesis.Oncotarget · 2016Article
- Sam68 functions as a transcriptional coactivator of the p53 tumor suppressor.Nucleic acids research · 2016Article
- Sam68 is Overexpressed in Epithelial Ovarian Cancer and Promotes Tumor Cell Proliferation.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Analysis of the interaction between host factor Sam68 and viral elements during foot-and-mouth disease virus infections.Virology journal · 2015Article
- The RNA-binding protein Sam68 regulates tumor cell viability and hepatic carcinogenesis by inhibiting the transcriptional activity of FOXOs.Journal of molecular histology · 2015Article
- Sam68 promotes cellular proliferation and predicts poor prognosis in esophageal squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Clinical significance of Sam68 expression in endometrial carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Sam68 is cleaved by caspases under apoptotic cell death induced by ionizing radiation.Journal of radiation research · 2015Article
- SAM68: Signal Transduction and RNA Metabolism in Human Cancer.BioMed research international · 2015Review
- High Sam68 expression predicts poor prognosis in non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014Article
- The transcriptional co-activator SND1 is a novel regulator of alternative splicing in prostate cancer cells.Oncogene · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe RNA-binding protein Sam68 has been implicated in a number of cellular processes, including transcription, RNA splicing and export, translation, signal transduction, cell cycle progression and replication of the human immunodeficiency virus and poliovirus. However, the precise impact it has on essential cellular functions remains largely obscure.
resultsIn this report we show that conditional overexpression of Sam68 in fibroblasts results in both cell cycle arrest and apoptosis. Arrest in G1 phase of the cell cycle is associated with decreased levels of cyclins D1 and E RNA and protein, resulting in dramatically reduced Rb phosphorylation. Interestingly, cell cycle arrest does not require the specific RNA binding ability of Sam68. In marked contrast, induction of apoptosis by Sam68 absolutely requires a fully-functional RNA binding domain. Moreover, the anti-cancer agent trichostatin A potentiates Sam68-driven apoptosis.
conclusionsFor the first time we have shown that Sam68, an RNA binding protein with multiple apparent functions, exerts functionally separable effects on cell proliferation and survival, dependent on its ability to bind specifically to RNA. These findings shed new light on the ability of signal transducing RNA binding proteins to influence essential cell function. Moreover, the ability of a class of anti-cancer therapeutics to modulate its ability to promote apoptosis suggests that Sam68 status may impact some cancer treatments.
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Registered trials
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.