ArticleHuman cell2022
ELK1 suppresses SYTL1 expression by recruiting HDAC2 in bladder cancer progression.
Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
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Who cites it
6 citing papers in PubMed.
- DUSP5 suppresses esophageal squamous cell carcinoma by counteracting macrophage-derived AREG-ERK1/2 signaling and disrupting an oncogenic ERK1/2-ELK1-DUSP5 feedback circuitry.Cell death & disease · 2026Article
- RNF168 promotes chronic colitis through ANXA7-mediated autophagy and NLRP3-driven pyroptosis.Apoptosis : an international journal on programmed cell death · 2026Article
- Synaptotagmin-like 5 is a potential biomarker and correlates with immune infiltrates in thyroid carcinoma.Journal of molecular histology · 2025Article
- Mechanistic Insights and Clinical Implications of ELK1 in Solid Tumors: A Narrative Review.Cells · 2025Review
- Elevated expression of ELK1 promotes breast cancer cell growth and correlates with poor prognosis of breast cancer patients.Annals of medicine and surgery (2012) · 2024Article
- WTAP enhances the instability of SYTL1 mRNA caused by YTHDF2 in bladder cancer.Histology and histopathology · 2024Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
ETS transcription factor (ELK1) stimulates the expression of genes at the onset of the cell cycle and participates in early developmental programming. Here, we investigated whether alterations of ELK1 lead to progression of bladder cancer (BCa), a main neoplasm of urinary tract, and clarified the function of ELK1 in BCa. Using the GEO database, we identified ELK1 as the most significantly overexpressed gene in BCa, which was substantiated in the acquired clinical samples and cells. Silencing of ELK1 inhibited the malignant phenotype of BCa cells. Further analysis revealed that ELK1 synergized with histone deacetylase 2 (HDAC2) to specifically bind to the synaptotagmin like 1 (SYTL1) promoter, thereby repressing SYTL1 transcription and protein expression. Depletion of SYTL1 reversed the repressive effects of ELK1 depletion on the malignant phenotype of BCa cells. Our in vitro findings were reproduced in vivo on a nude mouse tumorigenic model. Together, our results reveal that ELK1, through suppression of SYTL1 via HDAC2, supports the malignant phenotype of BCa cells.
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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.