Stromal Expression of Vimentin Predicts the Clinical Outcome of Stage II Colorectal Cancer for High-Risk Patients

Abstract

BackgroundIncreased expression of vimentin in tissue samples from patients with colorectal cancer (CRC) has been previously demonstrated, but its prognostic significance remains controversial, and the clinical significance for patients with stage II CRC is still unknown. The aim of this study was to evaluate the expression of vimentin in CRC and its potential prognostic significance.Material/MethodsWe analyzed vimentin expression in 203 CRC tissue samples from patients with stage II cancer using immunohistochemistry, and correlated the findings with clinicopathological patient features. CRC-specific survival (CSS) and disease-free survival (DFS) were analyzed using the Kaplan-Meier method. Univariate and multivariate analysis was performed using the Cox proportional hazards method for survival.ResultsVimentin expression was significantly correlated only with tumor (T) stage (p=0.024). Kaplan-Meier survival analysis indicated that vimentin expression could stratify the CSS and DFS of patients with stage II CRC at high risk (p=0.029, p=0.042, respectively), but not those of low-risk stage II patients (p=0.208, p=0.361, respectively). Univariate and multivariate analysis further revealed that stromal vimentin expression is an independent prognostic factor for CSS and DFS of high-risk stage II patients (p=0.043, p=0.022, respectively). Moreover, high-risk stage II patients with low stromal vimentin expression benefitted more from standard adjuvant chemotherapy than those with high stromal vimentin expression (CSS: p=0.012 vs. p=0.407; DFS: p=0.017 vs. p=0.420).ConclusionsOur study suggests that stromal vimentin expression is a promising indicator for survival prediction and adjuvant chemotherapy response in patients with stage II CRC with high-risk factors for recurrence.

c‐Myb promotes growth and metastasis of colorectal cancer through c‐fos‐induced epithelial‐mesenchymal transition

“…27 Molecularly, the EMT phenotype is characterized by downregulation of epithelial markers (E-cadherin) and upregulation of mesenchymal markers (N-cadherin, Vimentin and snail). 28,29 In hepatocellular carcinoma, c-Myb functions as a target of long non-coding RNA downregulated in hepatocellular carcinoma (DRHC) to promote the EMT phenotype through the MEK/ERK signaling pathway. 30 c-Myb could also cooperate with transforming growth factor beta (TGF-β) to enhance the EMT phenotype of estrogen(+) breast cancer cells.…”

High tumor cell vimentin expression indicatesprolonged survival in patients with ovarian malignant tumors

“…Numerous studies have revealed high vimentin expression as a negative prognostic factor in human neoplasms. In the case of colorectal cancer, it was shown that both tumor cell expression and tumor stroma expression were associated with poor patient prognosis [19,20,23]. In a meta-analysis by Du et al, vimentin expression indicated a shortened OS and disease-free survival (DFS), lymph node metastases, and a higher TNM stage of colorectal cancer patients [23].…”

“…To the best of our knowledge, our study is the first to report vimentin expression in the stroma of the ovarian neoplasm. We did identify studies showing that a poorer prognosis is related to stromal vimentin expression;but those studies concerned patients with colorectal and prostate cancers [20,29]. The tumor stroma mainly consists of resident fibroblasts, endothelial cells, pericytes, leukocytes, and extra-cellular matrix.…”

“…High expression of vimentin in cancer cells is associated with a poor prognosis for patients with numerous types of neoplasms. Recent studies have also emphasized that elevated stroma vimentin expression correlates with shortened survival rates in colorectal cancer patients [19,20].…”

Establishment of multiple diagnosis models for colorectal cancer with artificial neural networks

“…The clinical stage of disease is an indicator of prognosis for patients with CRC. Clinical stage I–II is considered early stage, while clinical stage III–IV is considered to be late stage (35,36).…”