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Carcinoma-associated fibroblasts (CAFs) play a pivotal role in promotingthe growth, invasion and metastasis of tumor cells. However, to date little isknown about the oncogenic mechanisms of CAFs. This study aimed to identify themicroenvironmental factors involved in tumor development and progression directedby CAFs in liver metastases. Tissue samples collected from 20 patients with colorectalliver metastases were used in this study. Histological and morphological characterizationof the samples was performed using hybridization and immunohistological assays.The mRNA expression of α-smooth muscle actin (α-SMA) was measured by northernblotting. The expression of plasminogen activator inhibitor type 1 (PAI-1) wasmeasured by enzyme-linked immunosorbent assay (ELISA). As a result, co-expressionof Thy-1 (CD90) and α-SMA was identified in CAFs, while normal liver samples werenegative for α-SMA and Thy-1. Compared with epidermal growth factor (EGF) andtumor necrosis factor (TNF) incubation, the expression of α-SMA increased significantlyfollowing transforming growth factor-1 (TGF-1) incubation (P&lt;0.05), while platelet-derivedgrowth factor (PDGF) caused a significant suppression of α-SMA expression (P&lt;0.05).PAI-1 expression was significantly lower in unstimulated fibroblasts comparedto TGF-1-treated fibroblasts (P&lt;0.01). The levels of PAI-1 transcription weresignificantly higher in CAFs from the patient samples compared with the healthycontrols. Taken together, our findings suggest that CAFs may be important in migration,matrix degradation, invasion and angiogenesis of tumors, and TGF-1 may promotethe activation of PAI-1 transcription in CAFs.

Transforming growth factor-1 promotes the transcriptional activation of plasminogen activator inhibitor type 1 in carcinoma-associated fibroblasts