ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
Downregulation of VGLL4 in the progression of esophageal squamous cell carcinoma.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Pooled it
- Aggressive high-grade NF2 mutant meningiomas downregulate oncogenic YAP signaling via the upregulation of VGLL4 and FAT3/4.bioRxiv : the preprint server for biology · 2024Article
- Clinical Significance and Expression Pattern of RIP5 and VGLL4 in Clear Cell Renal Cell Carcinoma Patients Treated with Sunitinib.Biomedicines · 2024Article
- Identification of Potential Biomarkers Using Integrative Approach: A Case Study of ESCC.SN computer science · 2023Article
- VGLL4 inhibits YAP1/TEAD signaling to suppress the epidermal squamous cell carcinoma cancer phenotype.Molecular carcinogenesis · 2021Article
- Article
- Multiple Roles of Vestigial-Like Family Members in Tumor Development.Frontiers in oncology · 2020Review
- Loss of VGLL4 suppresses tumor PD-L1 expression and immune evasion.The EMBO journal · 2019Article
- Zebrafish Vestigial Like Family Member 4b Is Required for Valvulogenesis Through Sequestration of Transcription Factor Myocyte Enhancer Factor 2c.Frontiers in cell and developmental biology · 2019Article
- Serotonin and YAP/VGLL4 Balance Correlated with Progression and Poor Prognosis of Hepatocellular Carcinoma.Scientific reports · 2018Article
- VGLL4 is a transcriptional cofactor acting as a novel tumor suppressor via interacting with TEADs.American journal of cancer research · 2018Review
- VGLL4 Selectively Represses YAP-Dependent Gene Induction and Tumorigenic Phenotypes in Breast Cancer.Scientific reports · 2017Article
- Hypoxia is a Key Driver of Alternative Splicing in Human Breast Cancer Cells.Scientific reports · 2017Article
- Identification of epigenetic interactions between miRNA and DNA methylation associated with gene expression as potential prognostic markers in bladder cancer.BMC medical genomics · 2017Article
- From vestigial to vestigial-like: the Drosophila gene that has taken wing.Development genes and evolution · 2016Review
- Ubiquitin-specific protease 11 (USP11) functions as a tumor suppressor through deubiquitinating and stabilizing VGLL4 protein.American journal of cancer research · 2016Article
- miR-222/VGLL4/YAP-TEAD1 regulatory loop promotes proliferation and invasion of gastric cancer cells.American journal of cancer research · 2015Article
- YAP-VGLL4 antagonism defines the major physiological function of the Hippo signaling effector YAP.Genes & developmentArticle
- Aggressive high-grade NF2 mutant meningiomas downregulate oncogenic YAP signaling via the upregulation of VGLL4 and FAT3/4.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
VGLL4, a member of the Vestigial-like (VGLL) proteins, has been reported to be dysregulated in several cancer types. However, its function in esophageal squamous cell carcinoma (ESCC) remains poorly understood. Here, it was found that the expression level of VGLL4 was decreased in ESCC tissues. Moreover, forced expression of VGLL4 in ESCC cells inhibited cell growth and migration, while knockdown of VGLL4 expression promoted the tumorigenecity of ESCC cells. Mechanistically, VGLL4 regulated the growth and motility of ESCC cells through downregulating the expression of connective tissue growth factor (CTGF), a known oncogene in the progression of ESCC. Taken together, our study suggested that downregulation of VGLL4 was very important in the progression of ESCC, and restoring the function of VGLL4 might be a promising therapeutic strategy for ESCC.
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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.