Insulin-like growth factor II mRNA-binding protein 3 (IMP3) is an oncofetal protein upregulated in tumor cells during carcinogenesis. The aim of the present study was to investigate the expression status of IMP3 in colorectal cancer (CRC) tissues and its clinical significance. Immunostaining was performed in 130 CRC samples, the association of IMP3 expression with clinicopathological characteristics was assessed and 58 patients were selected for survival analysis. To the best of our knowledge, the present study describes for the first time the expression of IMP3 in tumor stromal components of CRC. Stromal expression of IMP3 was detected in 24/130 (18.5%) CRC tissue specimens and was associated with tumor-node-metastasis (TNM) stage (stage III–IV, P=0.003), lymph node metastasis (P=0.006), lympho-vascular invasion (P=0.003), tumor border (P=0.013). Tumoral expression of IMP3 was detected in 94/130 (72.3%) of CRC specimens and was associated with T classification (T3-T4, P=0.027), tumor-node-metastasis (TNM) stage (stage III–IV, P=0.011), lymph node metastasis (P=0.048), tumor budding (>10 buds, P=0.005). Further study indicated that patients with IMP3 expressed in tumor cells and tumor stroma tend to have poorer overall survival rates (P=0.02 and P=0.06, respectively). Moreover, tumoral expression of IMP3 and TNM stage were identified to be independent prognostic factors in CRC. IMP3 was not only expressed in tumor cells but also in stroma cells. Stromal expression of IMP3 was associated with lymph node metastasis and advanced tumor TNM stage. Moreover, the survival analysis indicated that there is a significant association between IMP3 expression in tumor cells and a poorer overall survival rate in patients with CRC. The expression of IMP3 maybe a predicted factor for CRC patient.

Background: Inflammation is implicated in both hepatic cirrhosis development and hepatocellular carcinogenesis, and treatment with long-acting glucocorticoid dexamethasone prevented liver carcinogenesis in mice. However, it is unclear whether glucocorticoids have anti-inflammatory effect on hepatocellular carcinoma (HCC) and if short-acting glucocorticoids (with fewer adverse effects) inhibit paraneoplastic inflammation and HCC progression. Methods: To investigate whether different types of anti-inflammatory agents attenuate HCC progression, the current study compared effects of treatments with hydrocortisone (a shortacting glucocorticoid) or aspirin on HCC progression. HCC was induced in diethylnitrosaminetreated rats which were randomly divided into 4 groups (n=8), respectively receiving orally once daily vehicle, glucuronolactone, glucuronolactone+hydrocortisone, and glucuronolactone +aspirin. Diethylnitrosamine (DEN) was given to rats in drinking water (100mg/L) to induce HCC. At weeks 12 and 16 post-induction, effects were compared on HCC nodule formation, microvessel density, and macrophage infiltration, and levels of paraneoplastic protein expression of tumor necrosis factor (TNF)-α, p38 mitogen-activated protein kinase (p38), phosphorylated p38 (p-p38), nuclear factor (NF)-κB, interleukin (IL)-10, hepatocyte growth factor (HGF), transforming growth factor (TGF)-β1 and vascular endothelial growth factor (VEGF). Results: Compared to the model and glucuronolactone alone groups, HCC nodule number and microvessel density in the glucuronolactone+hydrocortisone group were significantly lower at week 12. At week 12 but not week 16, significantly lower levels of macrophages, TNF-α, p-p38, NF-κB, IL-10, HGF, TGF-β1 and VEGF were observed in the paraneoplastic tissue of the glucuronolactone+hydrocortisone group when compared with the control and glucuronolactone groups. Conclusion: The results suggest that hydrocortisone treatment reduces macrophage polarization, expression of inflammatory and anti-inflammatory cytokines, and angiogenesis in paraneoplastic tissue, and attenuates early HCC progression. Although hydrocortisone did not have attenuation effect on advanced solid tumor, the current study shows the potential benefits and supports potential clinical use of hydrocortisone in attenuating early progression of HCC, which is through suppressing paraneoplastic inflammation and angiogenesis.