Περίληψη:
The transforming growth factor beta (TGF-beta) signaling pathway has
been considered both a tumor suppressor and a cancer promoter.
Additionally, downregulation of cell adhesion molecules such as
E-cadherin plays an important role in the metastatic potential of
colorectal cancer (CRC). The aim of the present study was to evaluate
TGF-beta, TGF-beta type I receptor (TGF-beta R1), TGF-beta type II
receptor (TGF-beta R2), Smad4, pSmad2/3, and E-cadherin expression in
colorectal carcinoma and to correlate the obtained data with other
standard prognostic parameters, such as disease stage, metastases, and
patient survival. TGF-beta, TGF-beta R1, TGF-beta R2, Smad4, pSmad2/3,
and E-cadherin expression was evaluated immunohistochemically in 195
unrelated CRC specimens and the results subjected to various statistical
analyses. TGF-beta was expressed in 71.28%, TGF-beta R1 in 61.0%,
TGF-beta R2 in 54.4%, Smad4 in 61.5%, pSmad2/3 in 71.3%, and
E-cadherin in 50.26% of the colorectal carcinoma samples tested. The
correlation of immunoexpression with the clinicopathological parameters
of CRC revealed that the high expression of TGF-beta and low expression
of TGF-beta R1, TGF-beta R2, Smad4, pSmad2/3, and E-cadherin were
correlated with tumor-node-metastasis (TNM) stage of disease. High
TGF-beta expression and low TGF-beta R1, TGF-beta R2, Smad4, and
pSmad2/3 expression were also correlated with lymph node metastasis. The
Kaplan-Meier survival curves demonstrated a clear association of
cancer-specific overall survival with high TGF-beta, as well as low
TGF-beta R1, TGF-beta R2, Smad4, pSmad2/3, and E-cadherin expression.
Our results suggest that TGF-beta, TGF-beta R1, TGF-beta R2, Smad4,
pSmad2/3, and E-cadherin are closely related to TNM stage of CRC.
Moreover, TGF-beta, TGF-beta R2, Smad4, pSmad2/3, and E-cadherin emerge
as valuable independent biomarkers of prognosis in CRC patients.
Συγγραφείς:
Lampropoulos, Pavlos
Zizi-Sermpetzoglou, Adamantia
Rizos, Spyros
and Kostakis, Alkiviadis
Nikiteas, Nikolaos
Papavassiliou,
Athanasios G.
