ArticleMolecular and cellular biochemistry2016
Cytokeratin 18 is necessary for initiation of TGF-β1-induced epithelial-mesenchymal transition in breast epithelial cells.
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
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- Cytokeratin expression in breast cancer: from mechanisms, progression, diagnosis, and prognosis to therapeutic implications.Molecular & cellular oncology · 2025Review
- Tumour stemness and poor clinical outcomes in haemochromatosis patients with hepatocellular carcinoma.Journal of clinical pathology · 2024Article
- Lack of basic rationale in epithelial-mesenchymal transition and its related concepts.Cell & bioscience · 2024Review
- Synthesis of compounds based on the active domain of cabotegravir and their application in inhibiting tumor cells activity.ChemistryOpen · 2024Article
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- Roles of the cytoskeleton in human diseases.Molecular biology reports · 2023Review
- Vimentin and cytokeratin: Good alone, bad together.Seminars in cancer biology · 2022Review
- Genome-wide DNA hypermethylation opposes healing in patients with chronic wounds by impairing epithelial-mesenchymal transition.The Journal of clinical investigation · 2022Article
- Stearoyl-CoA desaturase 1 regulates malignant progression of cervical cancer cells.Bioengineered · 2022Article
- Prognostic prediction and immune infiltration analysis based on ferroptosis and EMT state in hepatocellular carcinoma.Frontiers in immunology · 2022Article
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- The Role of ATRA, Natural Ligand of Retinoic Acid Receptors, on EMT-Related Proteins in Breast Cancer: Minireview.International journal of molecular sciences · 2021Review
- Centromere protein U enhances the progression of bladder cancer by promoting mitochondrial ribosomal protein s28 expression.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Early detection of tumor cells in bone marrow and peripheral blood in a fast‑progressing gastric cancer model.International journal of oncology · 2021Article
- DIscBIO: A User-Friendly Pipeline for Biomarker Discovery in Single-Cell Transcriptomics.International journal of molecular sciences · 2021Article
- KRT18 Modulates Alternative Splicing of Genes Involved in Proliferation and Apoptosis Processes in Both Gastric Cancer Cells and Clinical Samples.Frontiers in genetics · 2021Article
- Gene expression profiling of fibroblasts in a family with LMNA-related cardiomyopathy reveals molecular pathways implicated in disease pathogenesis.BMC medical genetics · 2020Article
- Phosphorylation of keratin 18 serine 52 regulates mother-daughter centriole engagement and microtubule nucleation by cell cycle-dependent accumulation at the centriole.Histochemistry and cell biology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During epithelial-mesenchymal transition (EMT), epithelial cells lose key phenotypic markers (e.g., E-cadherin and cytokeratin 18) and acquire mesenchymal markers (e.g., N-cadherin and vimentin). Although the loss of cytokeratin 18 is a hallmark of EMT, the regulatory role of cytokeratin 18 in EMT is not yet fully understood. Here, we report that cytokeratin 18 is involved in the regulation of transforming growth factor-beta1 (TGF-β1)-induced EMT in breast epithelial cells. When MCF10A cells were treated with TGF-β1 for 24 h, considerable morphological changes, indicative of the early stages of EMT (e.g., loss of cell-cell contact), were observed and cytokeratin 18 was downregulated. However, E-cadherin levels were not altered until a later time point. This suggests that cytokeratin 18 may play an active role during the earlier stages of EMT. Consistent with this notion, siRNA-mediated knockdown of cytokeratin 18 delayed TGF-β1-mediated EMT, and the associated downregulation of E-cadherin reduced the phosphorylation/nuclear localization of smad 2/3 and decreased the expression levels of snail and slug (which inhibit E-cadherin expression in epithelial cells as an early response to TGF-β1). Taken together, these results suggest that cytokeratin 18 critically contributes to initiating TGF-β1-induced EMT via the smad 2/3-mediated regulation of snail and slug expression in breast epithelial cells.
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