MicroRNA-495 inhibits the progression of non-small-cell lung cancer by targeting TCF4 and inactivating Wnt/ß-catenin pathway.

OBJECTIVE: Different effects of microRNA-495 (miR-495) on human cancers have been exhibited in recent years. However, the specific function of miR-495 remains uncertain in non-small-cell lung cancer (NSCLC). Thus, we aim to explore the role of miR-495 in NSCLC. PATIENTS AND METHODS: The expressions of miR-495 and transcription factor 4 (TCF4) were detected through quantitative Real-time polymerase chain reaction (qRT-PCR) assay. Western blot was used to measure the protein expression of relative genes. The relationship between miR-495 and TCF4 was testified by the dual-luciferase reporter gene assay. The function of miR-495 was investigated through cell counting kit-8 (CCK-8) assay and transwell assay. RESULTS: MiR-495 was downregulated in NSCLC tissues. Overexpression of miR-495 inhibited the migration, invasion and proliferation of NSCLC cells. Further, TCF4 was a direct target gene of miR-495. TCF4 was highly expressed in NSCLC tissues. In addition, miR-495 inhibited the progression of NSCLC through targeting TCF4. Furthermore, miR-495 inhibited EMT and Wnt/ß-catenin pathway in NSCLC. CONCLUSIONS: MiR-495 inhibited the progression of NSCLC by targeting TCF4 and inactivating Wnt/ß-catenin pathway.

Circulating antibodies to p16 protein-derived peptides in breast cancer.

Overexpression of the p16 protein has been reported in breast cancer and may trigger the secretion of antibodies against itself. Circulating anti-p16 antibodies that were detected with a recombinant protein have been reported in breast cancer. The present study was designed to determine whether the levels of circulating IgG antibody to p16 protein-derived linear antigens are altered in breast cancer. An enzyme-linked immunosorbent assay (ELISA) was developed in-house to determine circulating IgG against peptide antigens derived from the p16 protein in 152 female breast cancer patients and 160 healthy female subjects. The Student's T-test revealed that breast cancer patients exhibited significantly higher levels of anti-p16 IgG antibody compared to control subjects (T=2.02, P=0.045). In addition, ductal cancer appeared to be the main type contributing to the increased levels of circulating anti-p16 antibodies (T=2.08, P=0.038). Of all four stages of breast cancer, stage I was associated with the highest levels of IgG antibody (T=2.02, P=0.045) and receiver operating characteristic (ROC) analysis demonstrated that the area under the ROC curve was 0.74 (95% confidence interval: 0.65-083) and that the sensitivity against a specificity of 90% was 30.3%. Therefore, the levels of circulating IgG antibody to the p16 protein may be a potential biomarker for early diagnosis of breast cancer.

[Pathological changes in allogenic skin in combined radiation-burn injury in rats].

Skin allografts were transplanted to rats inflicted with third degree burns of 15% of BSA alone or combined with 5 Gy gamma ray radiation. Histopathological, histochemical and ultrastructural changes of the allografts were examined at different postoperative periods. In burned rats, allografts began to be rejected on the 8th postoperative day, showing degeneration and necrosis of its epithelial cells. Only in one rat it survived on the 14th day (10%), and all allografts were rejected before the 19th day. In contrast to this, most allografts (60-80%) on the rats with combined injury survived well for a period of 29 days. Epithelial cells and collagen fibers of the allografts degenerated in 1 to 4 days postoperation, and recovered to near normal during 9 to 14 days. During 24 to 29 days postoperation, the epithelial cells and appendices appeared almost normal in texture except an infiltration of a few lymphocytes and monocytes. The restoration of degenerated collagen, however, was slower than that of degenerated epithelium. The result shows that the survival time of skin allografts in severe combined radiation burn injury is prolonged than that in burns.

Ultrastructural changes of bone marrow megakaryocytes in several types of injury.

Seventy-one dogs were used in this study. Bone marrow tissues were examined by LM and EM and the peripheral blood platelets were counted. On the basis of previous research, megakaryocytophagia in bone marrow was confirmed. It was also proved that neutrophilic granulocytes participate in the autophagocytosis reaction in the body. Megakaryocytophagia plays a major role in the elimination of degenerate megakaryocytes in the marrow. The pathological change in megakaryocytes is considered to be one of the important causes of decrease in number and impairment of function of the platelets in burn, blast injury and burn-blast combined injury.