No abstract

Background:The effective mechanisms of microRNAs (miRNAs) functions as oncogenes or tumour suppressors in human hepatocellular carcinoma (HCC) are still obscure. Here, we investigated the function and expression of miR-1228 in HCC.Methods:The role of miR-1228 in HCC was determined by colony formation, transwell, and nude mice xenograft experiments. miR-1228 target gene were identified by EGFP reporter assays, real-time PCR, and western blot analysis. Dual-luciferase reporter assay and real-time PCR analysis are used to examine the regulation of p53.Results:miR-1228 promoted proliferation and metastasis, and facilitated the transition of cell cycle in hepatoma cells. miR-1228 downregulated p53 expression by binding to its 3′UTR. The ectopic expression of p53 abrogated the phenotypes induced by miR-1228. An inverse correlation existed between miR-1228 and p53 expression in hepatoma tissues compared with the adjacent tissues and three hepatoma cell lines. Moreover, we found that p53 suppressed the expression and promoter activity of miR-1228.Conclusions:miR-1228 functions as an oncogene by promoting cell cycle progression and cell mobility and negatively regulates the expression of p53. p53 downregulation in turn leads to an increase in miR-1228 expression, thereby forming a positive feedback loop that contributes to cancerogenesis in HCC.

The use of PKC inhibitors in addition to chemotherapy was not a valid alternative for patients with advanced NSCLC.

Postoperative adjuvant TACE improves the survival of patients with HBV-related HCC (stage B) after curative resection compared to surgery only.

Tumour-infiltrating lymphocytes (TILs) have been found to play crucial roles in a series of cancers. However, the impact of these cells on gallbladder carcinoma (GBC) remains poorly understood. In this study, we examined infiltrating FoxP3+, IL-17+, CD4+ and CD8+ cells by immunohistochemistry in specimens of 104 patients with GBC and evaluated the association of these cells with clinicopathological features and prognosis. The number of FoxP3+ cells was increased in a stepwise manner from CC to GA and GBC (GA versus CC, P = 0.036; early GBC versus GA, P = 0.032; advanced versus early GBC, P = 0.025). Both intratumoral FoxP3+ and IL-17+ cells correlated with nodal metastasis and TNM stage. Additionally, there were more infiltrating FoxP3+ cells in specimens with distant metastasis (P = 0.014). The group with high FoxP3+ cells showed poor overall survival (OS, P < 0.001) and disease-free survival (DFS, P < 0.001), and high infiltration of IL-17-producing cells was also a predictor of poor OS (P = 0.024). Multivariate analysis revealed that the presence of intratumoral FoxP3+ cells was an independent prognostic indicator for poor DFS (P < 0.01). In summary, these findings indicate that FoxP3+ and IL-17+ cells cooperatively facilitate pathogenesis and progression of GBC and show prognostic significance for OS or DFS.