ArticleCell cycle (Georgetown, Tex.)2015
SIAH ubiquitin ligases regulate breast cancer cell migration and invasion independent of the oxygen status.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- E3 Ubiquitin Ligases in Breast Cancer Metastasis: A Systematic Review of Pathogenic Functions and Clinical Implications.Frontiers in oncology · 2021Pooled it
- TSG101 Promotes SIAH1 Auto-Ubiquitination to Drive Migration and Invasion in Hepatocellular Carcinoma Cells.Journal of cellular and molecular medicine · 2026Article
- Construction and validation of antibody dependent cell phagocytosis related risk model in breast cancer.Scientific reports · 2025Article
- Tumour hypoxia in driving genomic instability and tumour evolution.Nature reviews. Cancer · 2025Review
- Non-apoptotic regulatory cell death scoring system to predict the clinical outcome and drug choices in breast cancer.Heliyon · 2024Article
- Article
- Unique E2-binding specificity of artificial RING fingers in cancer cells.Scientific reports · 2024Article
- The Alliance Between the German Cancer Research Center and Bayer: A Retrospective of an Innovative Collaboration Model.Handbook of experimental pharmacology · 2024Review
- Artificial RING finger reveals unique auto-ubiquitination with E2 specificity.Protein science : a publication of the Protein Society · 2023Article
- Zooming into the structure-function of RING finger proteins for anti-cancer therapeutic applications.American journal of cancer research · 2023Review
- Correlation between Ubiquitin E3 Ligases (Iranian journal of public health · 2022Article
- Reactive oxygen species-induced SIAH1 promotes granulosa cells' senescence in premature ovarian failure.Journal of cellular and molecular medicine · 2022Article
- Expression of the preadipocyte marker ZFP423 is dysregulated between well-differentiated and dedifferentiated liposarcoma.BMC cancer · 2022Article
- Helicobacter pylori-induced gastric cancer is orchestrated by MRCKβ-mediated Siah2 phosphorylation.Journal of biomedical science · 2021Article
- Downregulation of Siah1 promotes colorectal cancer cell proliferation and migration by regulating AKT and YAP ubiquitylation and proteasome degradation.Cancer cell international · 2020Article
- Incorporating genetic networks into case-control association studies with high-dimensional DNA methylation data.BMC bioinformatics · 2019Article
- Unique auto-ubiquitination activities of artificial RING fingers in cancer cells.Protein science : a publication of the Protein Society · 2018Article
- SIAH and EGFR, Two RAS Pathway Biomarkers, are Highly Prognostic in Locally Advanced and Metastatic Breast Cancer.EBioMedicine · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Seven-in-absentia homolog (SIAH) proteins are evolutionary conserved RING type E3 ubiquitin ligases responsible for the degradation of key molecules regulating DNA damage response, hypoxic adaptation, apoptosis, angiogenesis, and cell proliferation. Many studies suggest a tumorigenic role for SIAH2. In breast cancer patients SIAH2 expression levels correlate with cancer aggressiveness and overall patient survival. In addition, SIAH inhibition reduced metastasis in melanoma. The role of SIAH1 in breast cancer is still ambiguous; both tumorigenic and tumor suppressive functions have been reported. Other studies categorized SIAH ligases as either pro- or antimigratory, while the significance for metastasis is largely unknown. Here, we re-evaluated the effects of SIAH1 and SIAH2 depletion in breast cancer cell lines, focusing on migration and invasion. We successfully knocked down SIAH1 and SIAH2 in several breast cancer cell lines. In luminal type MCF7 cells, this led to stabilization of the SIAH substrate Prolyl Hydroxylase Domain protein 3 (PHD3) and reduced Hypoxia-Inducible Factor 1α (HIF1α) protein levels. Both the knockdown of SIAH1 or SIAH2 led to increased apoptosis and reduced proliferation, with comparable effects. These results point to a tumor promoting role for SIAH1 in breast cancer similar to SIAH2. In addition, depletion of SIAH1 or SIAH2 also led to decreased cell migration and invasion in breast cancer cells. SIAH knockdown also controlled microtubule dynamics by markedly decreasing the protein levels of stathmin, most likely via p27(Kip1). Collectively, these results suggest that both SIAH ligases promote a migratory cancer cell phenotype and could contribute to metastasis in breast cancer.
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