ArticlePloS one2014
Coexpression of EpCAM, CD44 variant isoforms and claudin-7 in anaplastic thyroid carcinoma.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Anaplastic thyroid carcinoma: Clinicopathologic and immunohistochemical study of 144 cases with special emphasis on the spectrum of histologic features.Virchows Archiv : an international journal of pathology · 2026Article
- Cancer Stemness and Dedifferentiation in Anaplastic Thyroid Carcinoma: Insights into a Multigenic, Microenvironmental Network and the Role of CD44.Biomedicines · 2026Review
- EpCAM silencing suppresses aggressive phenotypes and induces partial redifferentiation in anaplastic thyroid cancer cells.PloS one · 2026Article
- CD44v6 expression in non-anaplastic thyroid carcinoma: characterization of candidates for targeted therapy.Thyroid research · 2025Article
- Differential expression profiles of immunoregulatory genes in anaplastic thyroid carcinomas with a coexistent papillary carcinoma component.Virchows Archiv : an international journal of pathology · 2025Article
- Activation of the AKT-mTOR pathway confers selpercatinib resistance in thyroid cancer cells harboring theBiochemistry and biophysics reports · 2025Article
- CD44 Variant Expression in Follicular Cell-Derived Thyroid Cancers: Implications for Overcoming Multidrug Resistance.Molecules (Basel, Switzerland) · 2025Review
- Identification of potential targetable genes in papillary, follicular, and anaplastic thyroid carcinoma using bioinformatics analysis.Endocrine · 2024Article
- Characterization of EpCAM in thyroid cancer biology by three-dimensional spheroids in vitro model.Cancer cell international · 2024Article
- Utilizing CD44v6 and V600EBRAF-mutation for in vitro targeted combination therapy of thyroid carcinomas.Heliyon · 2023Article
- Selection, characterization and in vivo evaluation of novel CD44v6-targeting antibodies for targeted molecular radiotherapy.Scientific reports · 2023Article
- Customizing cancer treatment at the nanoscale: a focus on anaplastic thyroid cancer therapy.Journal of nanobiotechnology · 2023Review
- Hypomethylation-mediated overexpression of ITGA2 stimulates cell invasion and migration of thyroid carcinoma.Histology and histopathology · 2023Article
- EpCAM-claudin-tetraspanin-modulated ovarian cancer progression and drug resistance.Cell adhesion & migration · 2020Article
- Shedding light on the EpCAM: An overview.Journal of cellular physiology · 2019Review
- Ping-Pong-Tumor and Host in Pancreatic Cancer Progression.Frontiers in oncology · 2019Review
- HORMAD2 methylation-mediated epigenetic regulation of gene expression in thyroid cancer.Journal of cellular and molecular medicine · 2018Article
- Emerging clinical significance of claudin-7 in colorectal cancer: a review.Cancer management and research · 2018Review
- Inhibition of X-linked inhibitor of apoptosis protein suppresses tumorigenesis and enhances chemosensitivity in anaplastic thyroid carcinoma.Oncotarget · 2017Article
- PATZ1 knockdown enhances malignant phenotype in thyroid epithelial follicular cells and thyroid cancer cells.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAnaplastic thyroid cancer is considered to be one of the most aggressive human malignancies, and the mean survival time after diagnosis is approximately six months, regardless of treatments. This study aimed to examine how EpCAM and its related molecules are involved in the characteristics of anaplastic thyroid carcinoma. METHODOLOGY/PRINCIPAL
findingsTwo differentiated thyroid cancer cell lines (TPC-1 and FTC-133), and two anaplastic thyroid cancer cell lines (FRO, ACT-1) were analyzed for expression of CD44 standard isoform (CD44s), CD44 variant isoforms, and EpCAM, and human aldehyde dehydrogenase-1 (ALDH1) enzymatic activity using flow cytometry. CD44s expression was higher in TPC-1 and FTC-133 than in the FRO and ACT-1, whereas ALDH1 activities were higher in FRO and ACT-1 than in TPC-1 and FTC-133. An inverse correlation between CD44s expression and ALDH1 activity was observed in all thyroid cancer cell lines. As for the expressions of CD44 variant isoforms, ACT-1 showed higher and FRO showed moderate CD44v6 expressions, whereas either TPC-1 or FTC-133 showed negative CD44v6 expression. EpCAM expressions in FRO and ACT-1 were higher than those in TPC-1 and FTC-133, and EpCAM expressions inversely correlated with those of CD44s. A positive correlation was observed between EpCAM expression and ALDH1 activity in thyroid cancer cell lines. In the RT-PCR analysis, the expression levels of EpCAM, caludin-7 and ALDH1 in FRO and ATC-1 cells were significantly higher than those in TPC-1 and FTC-133 cells. In clinical specimens of thyroid cancers, nuclear expression of EpCAM and high expression of CD44v6 were detected significantly more frequently in anaplastic carcinomas. CONCLUSIONS/SIGNIFICANCE: Our study suggests the possibility that EpCAM, together with CD44v6 and claudin-7 as well as ALDH1, may be involved in the development of the aggressive phenotype of anaplastic thyroid carcinoma. Our findings may suggest a novel therapeutic strategy for treatment of anaplastic thyroid carcinoma.
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