ArticleCarcinogenesis2014
Six1 promotes epithelial-mesenchymal transition and malignant conversion in human papillomavirus type 16-immortalized human keratinocytes.
Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Targeting sine oculis homeoprotein 1 (SIX1): A review of oncogenic roles and potential natural product therapeutics.Heliyon · 2024Review
- SIX1 and EWS/FLI1 co-regulate an anti-metastatic gene network in Ewing Sarcoma.Nature communications · 2023Article
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- Epithelial-mesenchymal transition and its transcription factors.Bioscience reports · 2022Review
- Dissecting the effects of androgen deprivation therapy on cadherin switching in advanced prostate cancer: A molecular perspective.Oncology research · 2022Review
- Establishment of multifactor predictive models for the occurrence and progression of cervical intraepithelial neoplasia.BMC cancer · 2020Article
- Identification of a Small-Molecule Inhibitor That Disrupts the SIX1/EYA2 Complex, EMT, and Metastasis.Cancer research · 2020Article
- Human Papillomavirus 16 E5 Inhibits Interferon Signaling and Supports Episomal Viral Maintenance.Journal of virology · 2020Article
- HPV16-transformed human keratinocytes depend on SIX1 expression for proliferation and HPV E6/E7 gene expression.Virology · 2019Article
- Increased Six1 expression in macrophages promotes hepatocellular carcinoma growth and invasion by regulating MMP-9.Journal of cellular and molecular medicine · 2019Article
- Muscle precursor cell movements in zebrafish are dynamic and require Six family genes.Development (Cambridge, England) · 2019Article
- SIX1 Activates STAT3 Signaling to Promote the Proliferation of Thyroid Carcinoma via EYA1.Frontiers in oncology · 2019Article
- Transcriptional Downregulation of miR-4306 serves as a New Therapeutic Target for Triple Negative Breast Cancer.Theranostics · 2019Article
- Stem Cell Properties of Normal Human Keratinocytes Determine Transformation Responses to Human Papillomavirus 16 DNA.Journal of virology · 2018Article
- Signaling pathways and mesenchymal transition in pediatric high-grade glioma.Cellular and molecular life sciences : CMLS · 2018Review
- The regulation of cytokine signaling by retinal determination gene network pathway in cancer.OncoTargets and therapy · 2018Review
- Six1 promotes colorectal cancer growth and metastasis by stimulating angiogenesis and recruiting tumor-associated macrophages.Carcinogenesis · 2017Article
- The retinal determination gene network: from developmental regulator to cancer therapeutic target.Oncotarget · 2016Review
- Integrated Genomic Analysis of Pancreatic Ductal Adenocarcinomas Reveals Genomic Rearrangement Events as Significant Drivers of Disease.Cancer research · 2016Article
- The Interaction Between Human Papillomaviruses and the Stromal Microenvironment.Progress in molecular biology and translational science · 2016Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Six1, a member of the Six family of homeodomain transcription factors, is overexpressed in various human cancers, and SIX1 overexpression is associated with tumor progression and metastasis. Six1 messenger RNA levels increase during in vitro progression of human papillomavirus type 16 (HPV16)-immortalized human keratinocytes (HKc/HPV16) toward a differentiation-resistant (HKc/DR) phenotype. In this study, we show that HKc/DR-overexpressing Six1 exhibited a more mesenchymal phenotype, as characterized by a fibroblastic appearance and increased invasion. We utilized Whole Human Genome Microarrays to explore the gene expression changes associated with Six1 overexpression in HKc/DR. We found that overexpression of Six1 downregulated epithelial-related genes and upregulated mesenchymal-related genes, which suggests that Six1 overexpression induces epithelial-mesenchymal transition (EMT). Pathway analysis of the microarray data showed alterations in the transforming growth factor-beta (TGF-β) pathway, including enhanced expression of the TGF-β receptor type II (TβRII), and activation of the mitogen-activated protein kinase (MAPK) pathway in HKc/DR-overexpressing Six1, suggesting that Smad-independent pathways of TGF-β signaling may be involved in Six1-mediated EMT. p38 MAPK activation was required for sustained Six1-induced EMT and TβRII overexpression. Finally, we determined that Six1 overexpression in HKc/DR resulted in malignant conversion and increased the cancer stem cell (CSC)-like population. Thus, Six1 overexpression promotes EMT, CSCs properties and malignant conversion in HKc/DR through MAPK activation, which supports the possible use of p38-TβRII inhibitors for the treatment of cancers overexpressing Six1.
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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.