ArticleScientific reports2020
Differential functions of ERK1 and ERK2 in lung metastasis processes in triple-negative breast cancer.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- Integrating dynamic modeling of signaling pathways with subject-specific transcriptomic data to assess breast cancer risk.PloS one · 2026Article
- SCAMP3-Driven Regulation of ERK1/2 and Autophagy Phosphoproteomics Signatures in Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Article
- Lysosome-dependent nutrient scavenging underlies stress adaptation during epithelial-to-mesenchymal transition.bioRxiv : the preprint server for biology · 2025Article
- Inhibition of MCL-1 and MEK Overcomes MEK Inhibitor Resistance in Triple-Negative and Inflammatory Breast Cancers.Molecular cancer therapeutics · 2025Article
- Tracing the molecular landscape of diabetic nephropathy: Insights from machine learning and experiment verification.Journal of diabetes investigation · 2025Article
- Comprehensive network pharmacology and experimental study to investigate the effect and mechanism of solasonine on breast carcinoma treatment.Cancer cell international · 2025Article
- Clinical Progress of Targeted Therapy for Breast Cancer: A Comprehensive Review.Current cancer drug targets · 2025Review
- Interdependency and differential expression of ERK1 and ERK2 in breast and melanoma cell lines.Journal of the Egyptian National Cancer Institute · 2024Article
- Molecular docking and dynamics studies to identify novel active compounds targeting potential breast cancer receptor proteins from an indigenous herbF1000Research · 2024Article
- A novel chemical genetic approach reveals paralog-specific role of ERK1/2 in mouse embryonic stem cell fate control.Frontiers in cell and developmental biology · 2024Article
- ERK2-topoisomerase II regulatory axis is important for gene activation in immediate early genes.Nature communications · 2023Article
- Lactate receptor GPR81 drives breast cancer growth and invasiveness through regulation of ECM properties and Notch ligand DLL4.BMC cancer · 2023Article
- The complex impact of cancer-related missense mutations on the stability and on the biophysical and biochemical properties of MAPK1 and MAPK3 somatic variants.Human genomics · 2023Article
- Computational Investigations on Reaction Mechanisms of the Covalent Inhibitors Ponatinib and Analogs Targeting the Extracellular Signal-Regulated Kinases.International journal of molecular sciences · 2023Article
- MAPK1 promotes the metastasis and invasion of gastric cancer as a bidirectional transcription factor.BMC cancer · 2023Article
- A cytotoxic effect of human lactoferrin fusion with Fc domain of IgG.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023Article
- Identification and biochemical characterization of small molecule inhibitors of ERK2 that target the D-recruitment site.Methods in enzymology · 2023Article
- Targeting Breast Cancer Stem Cells.International journal of biological sciences · 2023Review
- Opioids and immune checkpoint inhibitors differentially regulate a common immune network in triple-negative breast cancer.Frontiers in oncology · 2023Article
- Enhanced Therapeutic Effect of Optimized Melittin-dKLA, a Peptide Agent Targeting M2-like Tumor-Associated Macrophages in Triple-Negative Breast Cancer.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer characterized by metastasis, drug resistance and high rates of recurrence. With a lack or targeted therapies, TNBC is challenging to treat and carries a poor prognosis. Patients with TNBC tumors expressing high levels of ERK2 have a poorer prognosis than those with low ERK2-expressing tumors. The MAPK pathway is often found to be highly activated in TNBC, however the precise functions of the ERK isoforms (ERK1 and ERK2) in cancer progression have not been well defined. We hypothesized that ERK2, but not ERK1, promotes the cancer stem cell (CSC) phenotype and metastasis in TNBC. Stable knockdown clones of the ERK1 and ERK2 isoforms were generated in SUM149 and BT549 TNBC cells using shRNA lentiviral vectors. ERK2 knockdown significantly inhibited anchorage-independent colony formation and mammosphere formation, indicating compromised self-renewal capacity. This effect correlated with a reduction in migration and invasion. SCID-beige mice injected via the tail vein with ERK clones were employed to determine metastatic potential. SUM149 shERK2 cells had a significantly lower lung metastatic burden than control mice or mice injected with SUM149 shERK1 cells. The Affymetrix HGU133plus2 microarray platform was employed to identify gene expression changes in ERK isoform knockdown clones. Comparison of gene expression levels between SUM149 cells with ERK2 or ERK1 knockdown revealed differential and in some cases opposite effects on mRNA expression levels. Those changes associated with ERK2 knockdown predominantly altered regulation of CSCs and metastasis. Our findings indicate that ERK2 promotes metastasis and the CSC phenotype in TNBC.
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