Background & Objective: E-cadherin links to the cytoskeleton via catenins and mediates cell-cell homophilic adhesion. beta-catenin not only regulates cell-cell adhesion as a protein interacting with cadherin, but also functions as an important component of the Wnt signaling pathway which has been found to be closely associated with tumor formation. This study was performed to examine the expression of E-cadherin, beta-catenin, and cyclin D1 in breast cancer in order to evaluate their possible roles in the formation and progression of breast cancer.

Methods: The alterations of E-cadherin, beta-catenin, and cyclin D1 in 60 cases of breast cancer were determined using highly sensitive SP immunohistochemical method.

Results: Normal immunoreactivity of E-cadherin and beta-catenin were observed in 29 (48.3%) and 18 (30.0%) cases, respectively. Twenty-eight cases (46.7%) showed cyclin D1 overexpression. Thirty percent (9/29) of the cases with normal staining of E-cadherin showed overexpression of cyclin D1, while 61.3%(19/31) of the cases showed overexpression of cyclin D1 with abnormal staining of E-cadherin. Abnormal expression of E-cadherin and overexpression of cyclin D1 showed a significantly positive correlation (rs=0.303,P< 0.05). Forty-two cases showed abnormal staining of beta-catenin. Cyclin D1 overexpression was observed in 57.1% (24/42) of these cases with abnormal staining of beta-catenin, but only observed in 22.2% (4/18) of these cases with normal membranous staining of beta-catenin. There was a significantly positive correlation between the abnormal expression of beta-catenin and overexpression of cyclin D1 (rs=0.321, P< 0.05).

Conclusion: Down-regulation of E-cadherin and beta-catenin accumulation in the cytoplasm/nuclear may promote malignant transformation and progression by triggering cyclin D1 overexpression in breast cancer.

Download full-text PDF

Source

Publication Analysis

Top Keywords

e-cadherin beta-catenin
20
beta-catenin cyclin
16
overexpression cyclin
16
expression e-cadherin
12
breast cancer
12
cyclin overexpression
12
abnormal staining
12
staining beta-catenin
12
beta-catenin
10
cyclin
10

Similar Publications

SHP2 promotes the epithelial-mesenchymal transition in triple negative breast cancer cells by regulating β-catenin.

J Cancer Res Clin Oncol

January 2025

Key Laboratory of Laboratory Medicine, Ministry of Education of China, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.

Purpose: Growing evidence suggests that the tyrosine phosphatase SHP2 is pivotal for tumor progression. Triple-negative breast cancer (TNBC) is the most lethal subtype of breast cancer, characterized by its high recurrence rate, aggressive metastasis, and resistance to chemotherapy. Understanding the mechanisms of tumorigenesis and the underlying molecular pathways in TNBC could aid in identifying new therapeutic targets.

View Article and Find Full Text PDF

The epithelial-mesenchymal transition (EMT) assists in the acquisition of invasiveness, relapse, and resistance in non-small cell lung cancer (NSCLC) and can be caused by the signaling of transforming growth factor-β1 (TGF-β1) through Smad-mediated or Smad-independent pathways. (-)-Epigallocatechin-3-gallate (EGCG), a multifunctional cancer-preventing bioconstituent found in tea polyphenols, has been shown to repress TGF-β1-triggered EMT in the human NSCLC A549 cell line by inhibiting the activation of Smad2 and Erk1/2 or reducing the acetylation of Smad2 and Smad3. However, its impact on the Smad-independent pathway remains unclear.

View Article and Find Full Text PDF

Fusobacterium nucleatum modulates the Wnt/β-catenin pathway in colorectal cancer development.

Int J Biol Macromol

January 2025

Department of Molecular Biology and Biotechnology, University of Kalyani, Kalyani 741235, Nadia, West Bengal, India. Electronic address:

The Wnt/β-catenin signalling pathway normally maintains cellular and tissue homeostasis by regulating cellular differentiation and survival in a controlled manner. An aberrantly regulated Wnt/β-catenin signalling pathway can transform into an oncogenic pathway, which is associated with Colorectal cancer (CRC) as well as other cancers. CRC is one of the most frequently occurring gastrointestinal cancers worldwide.

View Article and Find Full Text PDF

Adult human hearts exhibit limited regenerative capacity. Post-injury cardiomyocyte (CM) loss can lead to myocardial dysfunction and failure. Although neonatal mammalian hearts can regenerate, the underlying molecular mechanisms remain elusive.

View Article and Find Full Text PDF

The trimeric intracellular cation channel B (TRIC-B), encoded by TMEM38B, is a potassium (K) channel present in the endoplasmic reticulum membrane, where it counterbalances calcium (Ca) exit. Lack of TRIC-B activity causes a recessive form of the skeletal disease osteogenesis imperfecta (OI), namely OI type XIV, characterized by impaired intracellular Ca flux and defects in osteoblast (OB) differentiation and activity. Taking advantage of the OB-specific Tmem38b knockout mouse (Runx2Cre;Tmem38b; cKO), we investigated how the ion imbalance affects the osteogenetic process.

View Article and Find Full Text PDF

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!