ArticleBMC cancer2013
Sox2 suppresses the invasiveness of breast cancer cells via a mechanism that is dependent on Twist1 and the status of Sox2 transcription activity.
Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- The Role of Small Interfering RNAs in Hepatocellular Carcinoma.Journal of gastrointestinal cancer · 2024Review
- SOX2 promotes a cancer stem cell-like phenotype and local spreading in oral squamous cell carcinoma.PloS one · 2023Article
- Article
- SOX2 and Bcl-2 as a Novel Prognostic Value in Hepatocellular Carcinoma Progression.Current oncology (Toronto, Ont.) · 2021Article
- Carcinoma-Associated Fibroblasts Promote Growth of Sox2-Expressing Breast Cancer Cells.Cancers · 2020Article
- Functional characterization of SOX2 as an anticancer target.Signal transduction and targeted therapy · 2020Review
- Kdm4c is Recruited to Mitotic Chromosomes and Is Relevant for Chromosomal Stability, Cell Migration and Invasion of Triple Negative Breast Cancer Cells.Breast cancer : basic and clinical research · 2018Article
- Modulation of SOX2 expression delineates an end-point for paclitaxel-effectiveness in breast cancer stem cells.Scientific reports · 2017Article
- Expression of sex-determining region Y-box protein 2 in breast cancer and its clinical significance.Saudi medical journal · 2017Review
- CMV70-3P miRNA contributes to the CMV mediated glioma stemness and represents a target for glioma experimental therapy.Oncotarget · 2017Article
- Oxidative stress induces the acquisition of cancer stem-like phenotype in breast cancer detectable by using a Sox2 regulatory region-2 (SRR2) reporter.Oncotarget · 2016Article
- Article
- Radioactive (125)I seeds inhibit cell growth and epithelial-mesenchymal transition in human glioblastoma multiforme via a ROS-mediated signaling pathway.BMC cancer · 2015Article
- Profiling gene promoter occupancy of Sox2 in two phenotypically distinct breast cancer cell subsets using chromatin immunoprecipitation and genome-wide promoter microarrays.Breast cancer research : BCR · 2014Article
- SOX2 and cancer: current research and its implications in the clinic.Clinical and translational medicine · 2014Review
- Nuclear reprogramming of luminal-like breast cancer cells generates Sox2-overexpressing cancer stem-like cellular states harboring transcriptional activation of the mTOR pathway.Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundSox2, an embryonic stem cell marker, is aberrantly expressed in a subset of breast cancer (BC). While the aberrant expression of Sox2 has been shown to significantly correlate with a number of clinicopathologic parameters in BC, its biological significance in BC is incompletely understood.
methodsIn-vitro invasion assay was used to evaluate whether the expression of Sox2 is linked to the invasiveness of MCF7 and ZR751 cells. Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and/or Western blots were used to assess if Sox2 modulates the expression of factors known to regulate epithelial mesenchymal transition (EMT), such as Twist1. Chromatin immunoprecipitation (ChIP) was used to assess the binding of Sox2 to the promoter region of Twist1.
resultsWe found that siRNA knockdown of Sox2 expression significantly increased the invasiveness of MCF7 and ZR751 cells. However, when MCF7 cells were separated into two distinct subsets based on their differential responsiveness to the Sox2 reporter, the Sox2-mediated effects on invasiveness was observed only in 'reporter un-responsive' cells (RU cells) but not 'reporter responsive' cells (RR cells). Correlating with these findings, siRNA knockdown of Sox2 in RU cells, but not RR cells, dramatically increased the expression of Twist1. Accordingly, using ChIP, we found evidence that Sox2 binds to the promoter region of Twist1 in RU cells only. Lastly, siRNA knockdown of Twist1 largely abrogated the regulatory effect of Sox2 on the invasiveness in RU cells, suggesting that the observed Sox2-mediated effects are Twist1-dependent.
conclusionSox2 regulates the invasiveness of BC cells via a mechanism that is dependent on Twist1 and the transcriptional status of Sox2. Our results have further highlighted a new level of biological complexity and heterogeneity of BC cells that may carry significant clinical implications.
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