ArticleOncogene2007
The RNA-binding protein Sam68 contributes to proliferation and survival of human prostate cancer cells.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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
106 citing papers in PubMed, 186 citations in OpenAlex.
- Mechanistic insights and clinical implications of RNA-binding proteins in prostate cancer.Discover oncology · 2026Review
- Human papillomavirus 16 E6 oncoprotein promotes up-regulation of RNA-binding protein Sam68 in head and neck cancer.Frontiers in microbiology · 2026Article
- Roles of KHDRBS2 and KHDRBS3 in prostate cancer progression and AR-V7 regulation.Discover oncology · 2025Article
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- Sam68 is a druggable vulnerability point in cancer stem cells.Cancer metastasis reviews · 2024Review
- Integrating proteomics and explainable artificial intelligence: a comprehensive analysis of protein biomarkers for endometrial cancer diagnosis and prognosis.Frontiers in molecular biosciences · 2024Article
- Validating Sam68 expression and protein level in breast cancer.Journal of medicine and life · 2023Article
- Cdk1-mediated threonine phosphorylation of Sam68 modulates its RNA binding, alternative splicing activity and cellular functions.Nucleic acids research · 2022Article
- RNA binding proteins (RBPs) and their role in DNA damage and radiation response in cancer.Advanced drug delivery reviews · 2022Review
- The transcriptional terminator XRN2 and the RNA-binding protein Sam68 link alternative polyadenylation to cell cycle progression in prostate cancer.Nature structural & molecular biology · 2022Article
- Role of Sam68 in Sunitinib induced renal cell carcinoma apoptosis.Cancer medicine · 2022Article
- DNA Damage Regulates the Functions of the RNA Binding Protein Sam68 through ATM-Dependent Phosphorylation.Cancers · 2022Article
- Article
- RNA-binding proteins in ovarian cancer: a novel avenue of their roles in diagnosis and treatment.Journal of translational medicine · 2022Review
- Shortening of the KHDRBS1 3'UTR by alternative cleavage and polyadenylation alters miRNA-mediated regulation and promotes gastric cancer progression.American journal of translational research · 2022Article
- Research progress on RNA-binding proteins in breast cancer.Frontiers in oncology · 2022Review
- RNA-Binding Protein COL14A1, TNS1, NUSAP1 and YWHAE Are Valid Biomarkers to Predict Peritoneal Metastasis in Gastric Cancer.Frontiers in oncology · 2022Article
- Sam68 contributes to intestinal inflammation in experimental and human colitis.Cellular and molecular life sciences : CMLS · 2021Article
- Identification and validation of seven RNA binding protein genes as a prognostic signature in oral cavity squamous cell carcinoma.Bioengineered · 2021Article
- The Role of HSPB8, a Component of the Chaperone-Assisted Selective Autophagy Machinery, in Cancer.Cells · 2021Review
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tyrosine kinase Src is frequently activated in advanced human prostate carcinomas and its activation correlates with tyrosine phosphorylation of the RNA-binding protein Sam68. Herein, we have investigated the expression and function of Sam68 in human prostate cancer cells. Analysis of specimens obtained from 20 patients revealed that Sam68 is upregulated at the protein level in 35% of the samples. Real-time polymerase chain reaction confirmed the results at the mRNA level in most patients. Downregulation of Sam68 by RNAi in LNCaP prostate cancer cells delayed cell cycle progression and reduced the proliferation rate. Moreover, depletion of Sam68 sensitized cells to apoptosis induced by DNA-damaging agents. Similarly, stable cell lines expressing a truncated GFP-Sam68(GSG) protein displayed reduced growth rates and higher sensitivity to cisplatin-induced apoptosis. Microarray analyses revealed that a subset of genes involved in proliferation and apoptosis were altered when Sam68 was knocked down in LNCaP cells. Our results indicate that Sam68 expression supports prostate cancer cells proliferation and survival to cytotoxic agents.
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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.