ArticleMolecular oncology2024
ALDH1A3 promotes invasion and metastasis in triple-negative breast cancer by regulating the plasminogen activation pathway.
Article in Molecular oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- An epithelial cell fate-driven predictive model for liver metastasis risk in primary colorectal cancer through single-cell and multi-omics integration.Journal of translational medicine · 2026Article
- Selective inhibition of ALDH1A3 impedes breast cancer growth and metastasis by blocking ALDH1A3-driven transcriptional programs.iScience · 2026Article
- Cancer stem cell markers, chemotherapy response, and survival in triple-negative breast cancer.World journal of clinical oncology · 2026Article
- Insufficient NNMT promotes autophagy and disrupts progesterone signaling in endometrial stromal cells in recurrent implantation failure by modulating the H3K9me3-ALDH1A3 pathway.Cell death discovery · 2025Article
- Autophagy-Related Proteins in Triple-Negative Breast Cancer: From Molecular Insights to Therapeutic Applications.International journal of molecular sciences · 2025Review
- A cross-sectional study on the expression of fibrinolytic system components and metalloproteinase-9 in women with early-stage and metastases breast cancer in Tucumán, Argentina.Einstein (Sao Paulo, Brazil) · 2025Article
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Authors and funding
17 authors at 1 institution in 2 countries.
Funding
Abstract
Aldehyde dehydrogenase 1A3 (ALDH1A3) is a cancer stem cell marker that promotes metastasis. Triple-negative breast cancer (TNBC) progression has been linked to ALDH1A3-induced gene expression changes. To investigate the mechanism of ALDH1A3-mediated breast cancer metastasis, we assessed the effect of ALDH1A3 on the expression of proteases and the regulators of proteases that degrade the extracellular matrix, a process that is essential for invasion and metastasis. This revealed that ALDH1A3 regulates the plasminogen activation pathway; it increased the levels and activity of tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA). This resulted in a corresponding increase in the activity of serine protease plasmin, the enzymatic product of tPA and uPA. The ALDH1A3 product all-trans-retinoic acid similarly increased tPA and plasmin activity. The increased invasion of TNBC cells by ALDH1A3 was plasminogen-dependent. In patient tumours, ALDH1A3 and tPA are co-expressed and their combined expression correlated with the TNBC subtype, high tumour grade and recurrent metastatic disease. Knockdown of tPA in TNBC cells inhibited plasmin generation and lymph node metastasis. These results identify the ALDH1A3-tPA-plasmin axis as a key contributor to breast cancer progression.
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Registered trials
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