β-catenin as a prognostic factor for prostate cancer (PCa)

Abstract

IntroductionThe prostate cancer is difficult to predict, and treatment failure is associated with local infiltration, as well as distant metastases. Adhesion and migration abilities to of cancer cells play a major role in formation of metastasis. The participation of β-catenin in pathogene-sis of many types of cancer and benign processes has been an important discovery of recent years.Material and methodsThe studied material was obtained by transrectal, sextant core biopsy from 102 patients hospitalized in Department of Urology, Regional Hospital in Kalisz (2001-2004).The aim of our study was to determine the predictive value of β-catenin immunoexpression in prostate cancer, to analyze the prognostic aspect of some histopathological features and finally to assess the relationship between β-catenin immunoreactivity and the microscopic image of the tumor.Relationships between the investigated variables were analyzed using the Chi2 test of compatibility. We used the Kaplan-Meier curves to assess survival differences between groups of patients. Finally we established which of the studied factors significantly affect the patient outcome, using the method of Cox proportional hazard regression.ResultsIn prostate cancer in comparison with the normal epithelium, both the location and the strength of β-catenin immunoexpression are impaired.ConclusionsOur results indicate that the presence of disorders in β-catenin immunoexpression in prostate cancer cells indicates a high risk of death due to tumor progression and makes it imperative for immediate treatment procedures.

Baicalin inhibits the metastasis of highly aggressive breast cancer cells by reversing epithelial-to-mesenchymal transition by targeting β-catenin signaling

“…Upon Wnt ligand engagement, β-catenin is activated and disrupted, followed by its translocation from the cytoplasm into the nucleus, where it facilitates the transcription of genes involved in EMT, such as Twist, Snail, Slug, which repress the expression of E-cadherin, influencing cell junction and polarity (37). Previous studies have reported that overexpression and hyperactivation of β-catenin are observed in aggressive basallike breast cancer, and are positively correlated with poor patient clinical outcome (38)(39)(40). Therefore, β-catenin may be a novel therapeutic target with which to overcome breast cancer metastasis and improve the prognosis of breast cancer patients.…”

CAPE suppresses migration and invasion of prostate cancer cells via activation of non-canonical Wnt signaling

“…Elevation of β-catenin and androgen receptor (AR) protein expression correlated with high Gleason grade, disease progression, and increasing serum prostate-specific antigen (PSA) levels in PCa patients [41]. The intensity of membrane associated β-catenin switched to cytoplasm was used to predict the higher risk of death in prostate cancer patients [42]. Our results revealed that CAPE treatment can significantly suppressed total and nuclear abundance of β-catenin (Figures 2, 3, 5), which may contribute to the inhibition of PCa metastasis caused by CAPE treatment.…”

P4HB modulates epithelial‑mesenchymal transition and the β‑catenin/Snail pathway influencing chemoresistance in liver cancer cells

“…Snail-induced EMT is partly due to the direct repression of E-cadherin transcription both during development and tumour progression (22). β-catenin serves a key role in regulating cell proliferation and differentiation (23,24). Epithelial integrity requires the stability of E-cadherin/β-catenin complexes (25).…”