ArticleThe Journal of surgical research2014
Schlafen 12 expression modulates prostate cancer cell differentiation.
Article in The Journal of surgical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Meta-analysis of global and high throughput public gene array data for robust vascular gene expression discovery in chronic rhinosinusitis: Implications in controlled release.Journal of controlled release : official journal of the Controlled Release Society · 2021Pooled it
- SLFN14 functions as a P-TEFb inhibitor to modulate the transcription of HIV-1 and cellular genes.Science advances · 2025Article
- Genetic ancestry concordant RNA splicing in prostate cancer involves oncogenic genes and associates with recurrence.NPJ precision oncology · 2025Article
- SLFN12 Expression Significantly Effects the Response to Chemotherapy Drugs in Triple-Negative Breast Cancer.Cancers · 2024Article
- Schlafen 12 Slows TNBC Tumor Growth, Induces Luminal Markers, and Predicts Favorable Survival.Cancers · 2023Article
- Progress in investigating the relationship between Schlafen5 genes and malignant tumors.Frontiers in oncology · 2023Review
- Structural, molecular, and functional insights into Schlafen proteins.Experimental & molecular medicine · 2022Review
- Structural and biochemical characterization of human Schlafen 5.Nucleic acids research · 2022Article
- 14-weeks combined exercise epigenetically modulated 118 genes of menopausal women with prediabetes.Frontiers in endocrinology · 2022Article
- Review
- Structure of PDE3A-SLFN12 complex reveals requirements for activation of SLFN12 RNase.Nature communications · 2021Article
- Human Schlafen 5 Inhibits Proliferation and Promotes Apoptosis in Lung Adenocarcinoma via the PTEN/PI3K/AKT/mTOR Pathway.BioMed research international · 2021Article
- Article
- A novel LncRNA transcript, RBAT1, accelerates tumorigenesis through interacting with HNRNPL and cis-activating E2F3.Molecular cancer · 2020Article
- Mechanistic insights into cancer cell killing through interaction of phosphodiesterase 3A and schlafen family member 12.The Journal of biological chemistry · 2020Article
- Deciphering the three-domain architecture in schlafens and the structures and roles of human schlafen12 and serpinB12 in transcriptional regulation.Journal of molecular graphics & modelling · 2019Article
- Article
- Schlafen12 Reduces the Aggressiveness of Triple Negative Breast Cancer through Post-Transcriptional Regulation of ZEB1 That Drives Stem Cell Differentiation.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019Article
- PDE3A inhibitor anagrelide activates death signaling pathway genes and synergizes with cell death-inducing cytokines to selectively inhibit cancer cell growth.American journal of cancer research · 2019Article
- Schlafen 12 Interaction with SerpinB12 and Deubiquitylases Drives Human Enterocyte Differentiation.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSchlafen proteins have previously been linked to leukocyte and intestinal epithelial differentiation. We hypothesized that Schlafen 12 (SLFN12) overexpression in human prostate epithelial cells would modulate expression of prostate-specific antigen (PSA) and dipeptidyl peptidase 4 (DPP4), markers of prostatic epithelial differentiation. MATERIALS AND
methodsDifferentiation of the human prostate cancer cell lines LNCaP and PC-3 was compared after infection with an adenoviral vector coding for SLFN12 (Ad-SLFN12) or green fluorescent protein (GFP) only expressing virus (control). Transcript levels of SLFN12, PSA, and DPP4 were evaluated by real-time reverse transcription PCR and protein levels by Western blotting. Because mixed lineage kinase (MLK) and one of its downstream effectors (extracellular signal-regulated kinases [ERK]) have previously been implicated in some aspects of prostate epithelial differentiation, we conducted further studies in which LNCaP cells were cotreated with dimethyl sulfoxide (control), PD98059 (ERK inhibitor), or MLK inhibitor during transfection with Ad-SLFN12 for 72 h.
resultsTreatment of LNCaP or PC-3 cells with Ad-SLFN12 reduced PSA expression by 56.6±4.6% (P<0.05) but increased DPP4 transcript level by 4.8±1.0 fold (P<0.05) versus Ad-GFP-treated controls. Further studies in LNCaP cells showed that Ad-SLFN12 overexpression increased the ratio of the mature E-cadherin protein to its precursor protein. Furthermore, SLFN12 overexpression promoted DPP4 expression either when MLK or ERK was blocked. ERK inhibition did not reverse SLFN12-induced changes in PSA, E-cadherin, or DPP4.
conclusionsSLFN12 may regulate differentiation in prostate epithelial cells, at least in part independently of ERK or MLK. Understanding how SLFN12 influences prostatic epithelial differentiation may ultimately identify targets to influence the phenotype of prostatic malignancy.
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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.