ArticleJournal of experimental & clinical cancer research : CR2021
MYLK4 promotes tumor progression through the activation of epidermal growth factor receptor signaling in osteosarcoma.
Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Phosphoproteome landscape of ARID1A and its implications in DNA damage response and breast cancer pathogenesis.Discover oncology · 2026Article
- Osimertinib inhibits the MYLK4-mediated phosphorylation of CDKAL1 to suppress stemness and chemoresistance in rhabdomyosarcoma.Signal transduction and targeted therapy · 2026Article
- Treating T24 cells with erianin restores gefitinib drug sensitivity by regulating MYLK to inhibit EGFR and EMT processes.American journal of cancer research · 2026Article
- Exploring the mechanism of action of astragaloside in the treatment of osteoarthritis based on network pharmacology.Biomedical engineering online · 2025Article
- Impact of ITH on PRAD patients and feasibility analysis of the positive correlation gene MYLK2 applied to PRAD treatment.Frontiers in genetics · 2025Article
- Loss of Pip4k2c confers liver-metastatic organotropism through insulin-dependent PI3K-AKT pathway activation.Nature cancer · 2024Article
- Circadian disruption dysregulates lung gene expression associated with inflammatory lung injury.Frontiers in immunology · 2024Article
- Epigenomic response to albuterol treatment in asthma-relevant airway epithelial cells.Clinical epigenetics · 2023Article
- Managing the immune microenvironment of osteosarcoma: the outlook for osteosarcoma treatment.Bone research · 2023Review
- Chlorinated benzothiadiazines inhibit angiogenesis through suppression of VEGFR2 phosphorylation.Bioorganic & medicinal chemistry · 2022Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOsteosarcoma (OS) is the most common primary bone cancer in adolescents and lung metastasis is the leading cause of death in patients with OS. However, the molecular mechanisms that promote OS growth and metastasis remain unknown.
methodsWe investigated the expression of myosin light chain kinase family members between metastasis and non-metastasis patients in the TARGET database and ensured that only myosin light chain kinase family member 4 (MYLK4) had higher expression in metastatic osteosarcoma patients. Then we confirmed the results by immunohistochemistry (IHC) and Western blotting (WB) of OS tissues. The effect of MYLK4 on the metastasis and proliferation of OS cells was investigated by wound healing, Transwell and colony-formation assays. Mass spectrum analysis was used to ensure the new binding protein of MYLK4. Tissue microarrays analysis was used to show the correlation between MYLK4 and pEGFR (Y1068). A series of in vivo experiments were conducted to reveal the mechanisms by which MYLK4 modulated the metastasis and proliferation of OS.
resultsMyosin Light Chain Kinase Family Member 4 (MYLK4) was significantly upregulated in metastatic human OS tissues. Growth and metastasis of OS could be accelerated by MYLK4 overexpression, whereas silencing MYLK4 expression resulted in decreased cell growth and metastasis. Mechanistically, mass spectrum analysis showed that MYLK4 interacted with the epidermal growth factor receptor (EGFR) in osteosarcoma cells and promoted growth and metastasis via the EGFR signaling pathway. Tissue microarrays analysis also showed that MYLK4 expression had a positive correlation with the expression of pEGFR (Y1068). Moreover, the EGFR inhibitor gefitinib could partially reverse the effect of cell proliferation and metastasis caused by MYLK4 overexpression. Importantly, the combination of MYLK4 and EGFR inhibitors had synergistic effects on growth and metastasis of OS in vitro and in vivo.
conclusionOur results indicate that MYLK4 promotes OS growth and metastasis by activating the EGFR signaling pathway and can be a novel therapeutic target for the treatment of OS patients.
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