ArticleCancer cell international2015
Transient knockdown-mediated deficiency in plectin alters hepatocellular motility in association with activated FAK and Rac1-GTPase.
Article in Cancer cell international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- The plakin family: Potential therapeutic targets for digestive system tumors.Journal of translational internal medicine · 2025Article
- The Role of Plectin Dysregulation in Cancer: Recent Advances.Molecules (Basel, Switzerland) · 2025Review
- Epiplakin expression dynamics during colon carcinogenesis: Correlation with proliferation.Biomolecules & biomedicine · 2024Article
- Plectin: Dual Participation in Tumor Progression.Biomolecules · 2024Review
- Role of plectin and its interacting molecules in cancer.Medical oncology (Northwood, London, England) · 2023Review
- Review
- The attributes of plakins in cancer and disease: perspectives on ovarian cancer progression, chemoresistance and recurrence.Cell communication and signaling : CCS · 2021Review
- The Expressions and Mechanisms of Sarcomeric Proteins in Cancers.Disease markers · 2020Review
- Unbiased peptoid combinatorial cell screen identifies plectin protein as a potential biomarker for lung cancer stem cells.Scientific reports · 2019Article
- Plectin protects podocytes from adriamycin-induced apoptosis and F-actin cytoskeletal disruption through the integrin α6β4/FAK/p38 MAPK pathway.Journal of cellular and molecular medicine · 2018Article
- Mammalian Plakins, Giant Cytolinkers: Versatile Biological Functions and Roles in Cancer.International journal of molecular sciences · 2018Review
- Plectin deficiency in liver cancer cells promotes cell migration and sensitivity to sorafenib treatment.Cell adhesion & migration · 2018Article
- The Prognostic Value of Cytokeratin and Sal-Like Protein 4 Expression in Hepatocellular Carcinoma and Intra-Hepatic Cholangiocarcinoma in Taiwan.International journal of medical sciences · 2018Article
- Cytokeratin 18-associated Histone 3 Modulation in Hepatocellular Carcinoma: A Mini Review.Cancer genomics & proteomicsReview
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPlectin is one of the cytolinker proteins that play a crucial role in maintaining the integrity of cellular architecture. It is a component of desmosome complexes connecting cytoskeletal proteins and trans-membrane molecules. In epithelial cells, plectin connects cytokeratins and integrin α6β4 in hemidesmosomes anchoring to the extracellular matrix. In addition to the function of molecular adherent, plectin has been reported to exhibit functions affecting cellular signals and responsive activities mediated by stress, cellular migration, polarization as well as the dynamic movement of actin filaments. Plectin deficiency in hepatocellular carcinoma results in abnormal expression of cytokeratin 18 and disassembled hemidesmosome. Therefore, it is hypothesized that the plectin deficiency-mediated collapse of cytoskeleton may modulate cellular motility that is associated with consequent metastatic behaviors of cancer cells. METHODS AND
resultsThe cellular motility of plectin-deficient Chang liver cells generated by transient knockdown were analyzed by trans-well migration assay and the results revealed a higher migration rate. The confocal microscopy also demonstrated less organized and more polarized morphology as well as more focal adhesion kinase activity in comparison with that of the mock Chang liver cells. Furthermore, plectin-knockdown in Chang liver cells was associated with a higher activity of Rac1-GTPase in accordance with the results of the Rac1 pull-down assay. The immunohistochemical assay on human hepatocellular carcinoma showed that the expression of focal adhesion kinase was increased in the invasive front of tumor.
conclusionPlectin-deficient human hepatic cells exhibit higher cell motility associated with increase in focal adhesion kinase activity that are comparable to the properties of invasive hepatocellular carcinoma.
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