ArticleClinical and experimental medicine2018
MYLK promotes hepatocellular carcinoma progression through regulating cytoskeleton to enhance epithelial-mesenchymal transition.
Article in Clinical and experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Prognostic Significance of Microvascular Invasion in Pancreatic Ductal Adenocarcinoma: A Systematic Review and Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021Pooled it
- Exosomal micro ribonucleic acid-154-5p derived from vascular smooth muscle cell mediates intracranial aneurysm phenotype in vitro via myosin light chain kinase targeting.The Journal of international medical research · 2026Article
- RHOV Is a Detachment-Responsive Rho GTPase Necessary for Ovarian Cancer Peritoneal Metastasis.Cancer research · 2026Article
- Immunoglobulin κ drives liver regeneration by stabilizing MYLK to maintain cytoskeletal integrity and promote hepatocyte proliferation.Journal of translational internal medicine · 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
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- Impact of ITH on PRAD patients and feasibility analysis of the positive correlation gene MYLK2 applied to PRAD treatment.Frontiers in genetics · 2025Article
- Targeting AGTPBP1 inhibits pancreatic cancer progression via regulating microtubules and ERK signaling pathway.Molecular medicine (Cambridge, Mass.) · 2024Article
- Development and experimental validation of an M2 macrophage and platelet-associated gene signature to predict prognosis and immunotherapy sensitivity in bladder cancer.Cancer science · 2024Article
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- Increased expression of phosphodiesterase 4 in activated hepatic stellate cells promotes cytoskeleton remodeling and cell migration.The Journal of pathology · 2023Article
- Elevation of Cytoplasmic Calcium Suppresses Microtentacle Formation and Function in Breast Tumor Cells.Cancers · 2023Article
- Identification of the hub genes associated with prostate cancer tumorigenesis.Frontiers in oncology · 2023Article
- Identification of candidate hub genes correlated with the pathogenesis, diagnosis, and prognosis of prostate cancer by integrated bioinformatics analysis.Translational cancer research · 2022Article
- Identification of key genes with prognostic value in gastric cancer by bioinformatics analysis.Frontiers in genetics · 2022Article
- CHD1L prevents lipopolysaccharide-induced hepatocellular carcinomar cell death by activating hnRNP A2/B1-nmMYLK axis.Cell death & disease · 2021Article
- HBO1 overexpression is important for hepatocellular carcinoma cell growth.Cell death & disease · 2021Article
- MYLK4 promotes tumor progression through the activation of epidermal growth factor receptor signaling in osteosarcoma.Journal of experimental & clinical cancer research : CR · 2021Article
- Discovery and validation of novel protein markers in mucosa of portal hypertensive gastropathy.BMC gastroenterology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Myosin light chain kinase (MYLK) is found to catalyze the phosphorylation of myosin light chains (MLC) and regulate invasion and metastasis in some malignancies. However, there is little knowledge on the role of MYLK in hepatocellular carcinoma (HCC), and no studies have been conducted to investigate the mechanisms underlying MYLK-mediated promotion of HCC invasion and metastasis until now. In this study, we investigated the expression of MYLK in 50 pairs of human HCC and adjacent liver specimens. High MYLK expression was significantly correlated with aggressive clinicopathological features including tumor encapsulation, microvascular invasion and metastasis. In vitro assays showed that shRNA-induced MYLK knockdown significantly inhibited the wound-healing ability of HCC cells and the ability to migrate and invade through Matrigel. We next uncovered that MYLK knockdown resulted in a reduction in the number of F-actin stress fibers, disorganization of F-actin architectures and morphological alterations of HCC cells. Phosphorylated MLC, rather than total MLC, was found to be markedly reduced in response to downregulation of MYLK expression, and MYLK-regulated actin cytoskeleton through phosphorylating MLC in HCC cells. In addition, Western blotting assay revealed downregulation of the epithelial marker E-cadherin and upregulation of mesenchymal markers Vimentin, N-cadherin and Snail. Taken together, our findings indicate that MYLK promotes HCC progression by altering cytoskeleton to enhance epithelial-mesenchymal transition (EMT).
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