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Colorectal cancer has an extremely poor prognosis due to its high rate of recurrence and metastasis. The present study aimed to investigate the correlations between the B7-H1 and B7-H4 expressions as well as the clinicopathological characteristics and the prognosis of patients with colorectal cancer. We further inferred from these findings whether T lymphocyte co-inhibitory molecules (B7-H1 and B7-H4) led to a poor prognosis in Heilongjiang patients with colorectal cancer. Survival analysis revealed that the poor prognosis of these patients was unrelated to patient age, tumor size or histological grade, or lymph node metastasis, but was associated with TNM stage, high B7-H1 and B7-H4 expression levels. High B7-H1 and B7-H4 expressions were closely correlated with poor prognosis in patients with colorectal cancer. We speculate that the joint detection of these molecules may clinically apply for diagnosing and predicting poor prognosis of patients with colorectal cancer in northeast China's Heilongjiang province. In addition, intervention of B7-H1 and B7-H4 may be beneficial for enhancement of immunity in these patients.

MicroRNAs (miRNAs) are a recently discovered class of small non-coding RNAs that regulate gene expression. miRNAs can contribute to cancer development and progression and are differentially expressed in normal tissue and cancer. In the present study, our aim was to investigate the expression of miR-155 in gastric cancer and to explore the mechanisms by which it influences gastric cancer cells. The level of miR-155 in 52 gastric carcinoma and corresponding non-tumor tissues was quantified by real-time reverse transcriptase-polymerase chain reaction. We used the data from EdU, CASY and cell adhesion assays to show how the expression of miR-155 affects viability and proliferation in SGC-7901 cancer cells. We also performed functional assays using the 3'-untranslated region (3'-UTR) of the c-myc gene as a miR-155 target in a luciferase reporter assay system. Our results indicated that miR-155 is downregulated in both human gastric carcinoma tissues and SGC-7901 cells. The high expression level of miR-155 may significantly downregulate cancer cell viability, proliferation and attachment. The level of miR-155 could influence endogenous c-myc expression in SGC-7901 cells, and may decrease its expression by binding to 3'-UTR of c-myc. In conclusion, our results suggest that miR-155 is extensively involved in the cancer pathogenesis of gastric carcinoma and support its function as recessive cancer genes. c-myc is an important miR-155 target gene.