ArticleOncology letters2016
Upregulation of SOX4 antagonizes cellular senescence in esophageal squamous cell carcinoma.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- NFATC2-mediated CST1 upregulation drives cholangiocarcinoma growth and metastasis.Cell death discovery · 2026Article
- Overexpression of SOX4 in MSCs inhibits cellular senescence and enhances therapeutic efficacy in systemic lupus erythematosus.Stem cell research & therapy · 2025Article
- Aging-associated mechanisms and metabolic vulnerabilities in esophageal carcinoma: an integrative review.Frontiers in cell and developmental biology · 2025Review
- THAP9-AS1/miR-133b/SOX4 positive feedback loop facilitates the progression of esophageal squamous cell carcinoma.Cell death & disease · 2021Article
- Clinical significance of vasculogenic mimicry, vascular endothelial cadherin and SOX4 in patients with esophageal squamous cell carcinoma.International journal of clinical and experimental pathology · 2019Article
- Evaluation of the correlativity of gender determining region Y-box 4, N-cadherin, CD44 and E-cadherin expression in the prognosis of esophageal squamous cell carcinoma.International journal of clinical and experimental pathology · 2019Article
- MicroRNA-338-3p targets SOX4 and inhibits cell proliferation and invasion of renal cell carcinoma.Experimental and therapeutic medicine · 2017Article
- Cigarette Smoke Mediates Nuclear to Cytoplasmic Trafficking of Transcriptional Inhibitor Kaiso through MUC1 and P120-Catenin.The American journal of pathology · 2016Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescence, a terminal cell proliferation arrest that is caused by a variety of cellular stresses such as telomere erosion, DNA damage and oncogenic signaling, is classically considered a tumor defense barrier. However, the mechanism by which cancer cells overcome senescence is undetermined. In this study, the gene expression array data of esophageal squamous cell carcinoma (ESCC) was compared with paired normal tissues and showed that a cohort of genes, including proteinases, chemokines and inflammation factors, are upregulated in ESCC, which exhibits the senescence-associated secretory phenotype. In addition, reverse transcription-quantitative polymerase chain reaction was used to demonstrate that gender determining region Y-box 4 (SOX4) is upregulated in ESCC, and that its expression is inversely correlated with senescence markers. In addition, the knockdown of SOX4 expression by short hairpin RNA decreases ESCC cell proliferation and enhances doxorubicin-induced cell senescence. These results reveal the presence of a senescent microenvironment in ESCC, and suggest an important antisenescence role of SOX4 in ESCC progression.
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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.