Epithelial-to-mesenchymal transition (EMT) has an active role in the malignant progression of epithelial tumor cells. The aim of the study was to identify the existence of the EMT mechanism in brain metastasis. Tumors from 29 patients with brain metastases were assessed in terms of the immunoexpression of EMT-related factors including Slug, ZEB1, ZEB2, and E-cadherin in tumor cells and the surrounding mesenchymal stromal cells. The results were compared between primary tumors and their matched metastatic brain tumors. Analysis of tumor cell expression showed that Slug, ZEB1, or ZEB2 expression was found in more than 10% of the neoplastic cells in the metastatic lesions of 17 cases (59%) and in the primary lesions of 7 cases (24%, P=0.02). The expression level of ZEB2 was negatively correlated with that of E-cadherin (P=0.05). There were no differences in the tumoral expression levels of Slug, ZEB1, or ZEB2 among the primary organs. Analysis of stromal cell expression revealed a global increase in ZEB1 and ZEB2 expression levels with metastases (P<0.0001). Quantitative analysis confirmed that messenger RNA expression of ZEB1 and ZEB2 was elevated in metastatic lesions. The increased expression of EMT-related factors in brain metastasis was found not only in tumor cells, but also in tumor-associated stromal cells. Our results suggest that EMT-related factors play a role as a facilitator of brain metastasis.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jocn.2017.08.050 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Roles of ZEB1 and ZEB2 in E-cadherin expression and cell aggressiveness in head and neck cancer.
Genes Cells
December 2024
Department of Biochemistry, University of Yamanashi, Chuo, Yamanashi, Japan.
Article Synopsis
- ZEB1 is a crucial factor in cancer cell behavior, particularly in differentiation and metastasis, while the role of ZEB2 in head and neck squamous cell carcinoma (HNSCC) is less understood.
- In experiments with mouse oral cancer (MOC) cells, both ZEB1 and ZEB2 overexpression led to a loss of epithelial traits and promoted aggressive cell behaviors.
- Interestingly, ZEB1 overexpression was found to increase ZEB2 levels and vice versa, but ZEB2 exhibited greater potential for aggressive growth than ZEB1 in lab conditions.
Relationship of Signaling Pathways between RKIP Expression and the Inhibition of EMT-Inducing Transcription Factors SNAIL1/2, TWIST1/2 and ZEB1/2.
Cancers (Basel)
September 2024
Department of Microbiology, Immunology & Molecular Genetics, David Geffen School of Medicine, Jonsson Comprehensive Cancer Center, University of California at Los Angeles, Los Angeles, CA 90095, USA.
Untreated primary carcinomas often lead to progression, invasion and metastasis, a process that involves the epithelial-to-mesenchymal transition (EMT). Several transcription factors (TFs) mediate the development of EMT, including SNAIL1/SNAIL2, TWIST1/TWIST2 and ZEB1/ZEB2, which are overexpressed in various carcinomas along with the under expression of the metastasis suppressor Raf Kinase Inhibitor Protein (RKIP). Overexpression of RKIP inhibits EMT and the above associated TFs.
View Article and Find Full Text PDFCharacteristics and transcriptional regulators of spontaneous epithelial-mesenchymal transition in genetically unperturbed patient-derived non-spindled breast carcinoma.
Breast Cancer Res
September 2024
Department of Oncology, National Taiwan University Hospital, No. 1, Changde St., Zhongzheng District, Taipei City, Taiwan.
Background: Although tumor cells undergoing epithelial-mesenchymal transition (EMT) typically exhibit spindle morphology in experimental models, such histomorphological evidence of EMT has predominantly been observed in rare primary spindle carcinomas. The characteristics and transcriptional regulators of spontaneous EMT in genetically unperturbed non-spindled carcinomas remain underexplored.
Methods: We used primary culture combined with RNA sequencing (RNA-seq), single-cell RNA-seq (scRNA-seq), and in situ RNA-seq to explore the characteristics and transcription factors (TFs) associated with potential spontaneous EMT in non-spindled breast carcinoma.
[Effect and mechanism of Compound Shougong Powder in attenuating triple-negative breast cancer progression by reversing epithelial-to-mesenchymal transition].
Zhongguo Zhong Yao Za Zhi
July 2024
School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine Hefei 230012, China Institute of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine Hefei 230012, China.
The study investigated the effect of Compound Shougong Powder(CSGP) on the biological functions of triple-negative breast cancer(TNBC) cells and whether its mechanism of action was related to the epithelial-mesenchymal transition(EMT) signaling pathway. TNBC cells(MDA-MB-231 and BT-549) were treated with different concentrations of CSGP-containing serum. MTS assay was used to detect the effect of CSGP on the proliferation of TNBC cells.
View Article and Find Full Text PDFComparison of serum levels of IL-10 and IL-11 and mRNA expression of IL-10, IL-11, COX-2, BCL6, and ZEB Family in peripheral blood mononuclear cells (PBMC) of women with polycystic ovary syndrome and healthy individuals.
J Reprod Immunol
August 2024
Department of Clinical Biochemistry, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran. Electronic address:
Background: The roles of IL-10, IL-11, COX-2, BCL6, ZEB1, and ZEB2 genes in the potential correlation between polycystic ovary syndrome (PCOS), inflammation, and cancer remain controversial.
Aims: This study aimed to compare serum levels of IL-10 and IL-11 and gene expression of IL-10, IL-11, COX-2, BCL6, ZEB1, and ZEB2 in PBMCs of women with PCOS and healthy controls.
Methods: A case-control study included 40 women with PCOS as the case group and 40 healthy women as controls.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!