Expression pattern of p‑Smad2/Smad4 as a predictor of survival in invasive breast ductal carcinoma

Abstract

The present study examined SMAD family member 4 (Smad4), SMAD family member 2 (Smad2) and phosphorylated (p-)Smad2 expression in biopsy specimens from patients with invasive breast ductal carcinoma, in order to assess their abilities as prognostic markers. A total of 126 tissue samples were selected, and the expression of Smad2, p-Smad2 and Smad4 in carcinoma tissues was detected by immunostaining, and the association between protein expression and clinicopathological variables was analyzed. Smad4 expression was negatively correlated with human epidermal growth factor receptor 2 in carcinoma tissues, and Smad4 expression was consistent with that of p-Smad2. Although multivariate analysis revealed that Smad2, p-Smad2 and Smad4 were not independent predictors, Kaplan-Meier curves demonstrated that Smad4 positivity was correlated with a longer overall survival (OS) and progression-free survival (PFS) time. However, upon analysis of combined markers, there was a significant difference between the p-Smad2/Smad4 co-positive and co-negative patients; the latter tended to exhibit a shorter OS and PFS time, and multivariate analysis revealed that the combined expression of p-Smad2 and Smad4 may be used as an independent prognostic factor. These results suggested that the assessment of p-Smad2 and Smad4 protein expression in breast ductal carcinoma biopsy specimens may provide additional prognostic information.

CAMSAP1 Mutation Correlates With Improved Prognosis in Small Cell Lung Cancer Patients Treated With Platinum-Based Chemotherapy

“…This is an important pathway affecting cell proliferation, differentiation and apoptosis, with the inhibition of Smad2 being shown to promote tumor metastasis (Ying et al, 2017). The expression of phosphorylated Smad2 (p-Smad2) is consistent with that of Smad4 in that a decrease in expression results in platinum resistance and poor prognosis (Huang et al, 2015;Liu et al, 2020;Wang et al, 2021). In both cases, this is due to the regulation of cell proliferation, adhesion and immune response.…”

Analysis of Gene Expression of miRNA-106b-5p and TRAIL in the Apoptosis Pathway in Gastric Cancer

“…In a more refined analysis, the miRWalk databases were used to determine validated targets miR-106b-5p genes involved in gastric carcinogenesis and 14 genes from this pathway were found: APC (regulator of the WNT signaling pathway), CCND1 (cyclin D1) CDKN1A (cyclin-dependent kinase inhibitor 1), E2F1, E2F2, E2F3 (transcription factor 1, 2, and 3, respectively), FZD9 (frizzled class receptor 9), MAPK1 (mitogen-activated protein kinase 1), MYC (proto-oncogene BHLH transcription factor), RB1 (transcriptional corepressor 1), SMAD4 (SMAD family member 4), TCF7L2 (transcription factor 7-like 2), TGFBR2 (transforming growth factor β receptor 2), and TP53 (tumor protein p53). Considering the main functions described in the process of carcinogenesis, these genes are involved in cell cycle regulation and tumor progression, cell growth, adhesion and migration, proliferation, differentiation, genome stability, DNA repair, and apoptosis [42][43][44][45][46][47][48][49].…”

Integrated TCGA and GEO analysis showed that SMAD7 is an independent prognostic factor for lung adenocarcinoma

“…Although SMAD4 cannot be used as an independent prognostic factor, it can be used as an independent prognostic factor in combination with p-SMAD2. [ 38 ] For SMAD5, it has been reported that miR-145 can promote the migration and migration of esophageal cancer cells by inhibiting theexpression of SMAD5. [ 39 ] Fstl1 can promote glioma growth through SMAD1/SMAD5/SMAD8.…”