ArticleOncogene2020
Loss of the Ste20-like kinase induces a basal/stem-like phenotype in HER2-positive breast cancers.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
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- SOX9: an important factor in regulating breast cancer.European journal of medical research · 2025Review
- IsopretGO-analysing and visualizing the functional consequences of differential splicing.NAR genomics and bioinformatics · 2024Article
- Identify characteristics of Vietnamese oral squamous cell carcinoma patients by machine learning on transcriptome and clinical-histopathological analysis.Journal of dental sciences · 2024Article
- Proteogenomic analysis reveals non-small cell lung cancer subtypes predicting chromosome instability, and tumor microenvironment.Nature communications · 2024Article
- CEACAM1 is a direct SOX10 target and inhibits melanoma immune infiltration and stemness.iScience · 2022Article
- Periostin gene expression in neu-positive breast cancer cells is regulated by a FGFR signaling cross talk with TGFβ/PI3K/AKT pathways.Breast cancer research : BCR · 2021Article
- Ste20-like Kinase Is Critical for Inhibitory Synapse Maintenance and Its Deficiency Confers a Developmental Dendritopathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- AKT-mediated phosphorylation of Sox9 induces Sox10 transcription in a murine model of HER2-positive breast cancer.Breast cancer research : BCR · 2021Article
- AKT-mediated regulation of chromatin ubiquitylation and tumorigenesis through Mel18 phosphorylation.Oncogene · 2021Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
HER2 is overexpressed in 20-30% of all breast cancers and is associated with an invasive disease and poor clinical outcome. The Ste20-like kinase (SLK) is activated downstream of HER2/Neu and is required for efficient epithelial-to-mesenchymal transition, cell cycle progression, and migration in the mammary epithelium. Here we show that loss of SLK in a murine model of HER2/Neu-positive breast cancers significantly accelerates tumor onset and decreases overall survival. Transcriptional profiling of SLK knockout HER2/Neu-derived tumor cells revealed a strong induction in the triple-negative breast cancer marker, Sox10, accompanied by an increase in mammary stem/progenitor activity. Similarly, we demonstrate that SLK and Sox10 expression are inversely correlated in patient samples, with the loss of SLK and acquisition of Sox10 marking the triple-negative subtype. Furthermore, pharmacological inhibition of AKT reduces SLK-null tumor growth in vivo and is rescued by ectopic Sox10 expression, suggesting that Sox10 is a critical regulator of tumor growth downstream of SLK/AKT. These findings highlight a role for SLK in negatively regulating HER2-induced mammary tumorigenesis and provide mechanistic insight into the regulation of Sox10 expression in breast cancer.
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