ArticleNucleic acids research2019
c-MYC empowers transcription and productive splicing of the oncogenic splicing factor Sam68 in cancer.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Promoter identity shapes splicing outcomes and fidelity.Nature communications · 2026Article
- HnRNP C binding to invertedScience advances · 2026Article
- Dishevelled-1 regulates global transcriptomic changes and associates with ETS1 transcription factor.Nature communications · 2025Article
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- SOX2 interacts with hnRNPK to modulate alternative splicing in mouse embryonic stem cells.Cell & bioscience · 2024Article
- Splicing targeting drugs highlight intron retention as an actionable vulnerability in advanced prostate cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Therapeutic potential of anti-PIK3CG treatment for multiple myeloma via inhibiting c-Myc pathway.Heliyon · 2024Article
- Oncometabolite lactate enhances breast cancer progression by orchestrating histone lactylation-dependent c-Myc expression.Translational oncology · 2023Article
- The RNA-binding proteins hnRNP H and F regulate splicing of a MYC-dependent HRAS exon in prostate cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- How Driver Oncogenes Shape and Are Shaped by Alternative Splicing Mechanisms in Tumors.Cancers · 2023Review
- 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
- The androgen receptor couples promoter recruitment of RNA processing factors to regulation of alternative polyadenylation at the 3' end of transcripts.Nucleic acids research · 2022Article
- Molecular mechanisms by which splice modulator GEX1A inhibits leukaemia development and progression.British journal of cancer · 2022Article
- Effective targeting of breast cancer stem cells by combined inhibition of Sam68 and Rad51.Oncogene · 2022Article
- Prognostic and therapeutic significance of COP9 signalosome subunit CSN5 in prostate cancer.Oncogene · 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
- Comparison of a Personalized Prostate Biopsy Pattern With Traditional Transrectal Prostate Biopsy: Different Cancer Detection Rate.Frontiers in cell and developmental biology · 2022Article
- Prognostic value ofFrontiers in genetics · 2022Article
- Identification of ZDHHC1 as a Pyroptosis Inducer and Potential Target in the Establishment of Pyroptosis-Related Signature in Localized Prostate Cancer.Oxidative medicine and cellular longevity · 2022Article
- RNA polymerase II speed: a key player in controlling and adapting transcriptome composition.The EMBO journal · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The splicing factor Sam68 is upregulated in many human cancers, including prostate cancer (PCa) where it promotes cell proliferation and survival. Nevertheless, in spite of its frequent upregulation in cancer, the mechanism(s) underlying its expression are largely unknown. Herein, bioinformatics analyses identified the promoter region of the Sam68 gene (KHDRBS1) and the proto-oncogenic transcription factor c-MYC as a key regulator of Sam68 expression. Upregulation of Sam68 and c-MYC correlate in PCa patients. c-MYC directly binds to and activates the Sam68 promoter. Furthermore, c-MYC affects productive splicing of the nascent Sam68 transcript by modulating the transcriptional elongation rate within the gene. Importantly, c-MYC-dependent expression of Sam68 is under the tight control of external cues, such as androgens and/or mitogens. These findings uncover an unexpected coordination of transcription and splicing of Sam68 by c-MYC, which may represent a key step in PCa tumorigenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.