Expression and Clinical Significance of Ki67 and SOX2 in Colorectal Cancer.

The purpose of the paper is to explore the expression levels and clinical significance of Ki67 and sex-determining region Y-box 2 (SOX2) in colorectal cancer. From January 2013 to December 2016, 176 patients with colorectal cancer who were pathologically diagnosed after surgery in the Department of General Surgery in Xiamen Chinese Medical Hospital are included in this study. The pathological parameters, including gender, age, pathological stage, depth of tumor invasion, lymph node metastasis, and distant metastasis, are recorded. Immunohistochemistry is used to detect the correlation between Ki67 and Sox2 protein expression and clinicopathological parameters in colorectal cancer. Immunohistochemistry shows that in each stage of colorectal cancer, the positive rate of SOX2 is higher than that of Ki67, and the sensitivity of SOX2 is relatively high. Moreover, the levels of Ki67 and SOX2 in the cancerous tissues are not related to gender, age, lymph node metastasis and distant metastasis (p > 0.05).

Overexpression of COUP­TFII suppresses proliferation and metastasis of human gastric cancer cells.

The abnormal expression of the chicken ovalbumin upstream promoter transcription factor 2 (COUP­TFII) is associated with numerous forms of cancer, including gastric, prostate, colon and lung cancer. However, previous studies investigating the association between COUP­TFII expression and the occurrence, recurrence, invasion and metastasis of gastric cancer are limited in number. In the present study, it was revealed that the expression of COUP­TFII is significantly reduced in gastric carcinoma tissues compared with normal gastric mucosa cells (GES­1). In addition, the expression of COUP­TFII was also reduced in gastric cancer cell lines compared with GES­1 cells. Furthermore, it was revealed that ectopic expression of COUP­TFII was able to suppress the proliferation, migration and invasion of gastric cells, as well as inhibit hepatic metastasis, in vivo. In addition, it was demonstrated that COUP­TFII knockdown was able to promote the proliferation, migration and invasion of GES­1 cells in vitro. Furthermore, database analysis suggested that COUP­TFII expression in patients with gastric cancer is correlated with clinical stage classification and increased expression levels of COUP­TFII improved overall survival rates in patients with gastric cancer. The results of the present study suggest that COUP­TFII functions as a significant regulatory suppressor of gastric cancer growth and metastasis, and suggests that COUP­TFII may serve as a novel diagnostic and prognostic biomarker for gastric cancer metastasis.

MiR-33a suppresses breast cancer cell proliferation and metastasis by targeting ADAM9 and ROS1.

MicroRNAs (miRNAs) are small noncoding RNAs that have a pivotal role in the post-transcriptional regulation of gene expression by sequence-specifically targeting multiple mRNAs. Although miR-33a was recently reported to play an important role in lipid homeostasis, atherosclerosis, and hepatic fibrosis, the functions of miR-33a in tumor progression and metastasis are largely unknown. Here, we found that downregulated miR-33a in breast cancer tissues correlates with lymph node metastasis. MiR-33a expression is significantly lower in the highly metastatic breast cancer cell lines than the noncancerous breast epithelial cells and non-metastatic breast cancer cells. Moreover, the overexpression of miR-33a in metastatic breast cancer cells remarkably decreases cell proliferation and invasion in vitro and significantly inhibits tumor growth and lung metastasis in vivo, whereas its knockdown in non-metastatic breast cancer cells significantly enhances cell proliferation and invasion in vitro and promotes tumor growth and lung metastasis in vivo. Combining bioinformatics prediction and biochemical analyses, we showed that ADAM9 and ROS1 are direct downstream targets of miR-33a. These findings identified miR-33a as a negative regulator of breast cancer cell proliferation and metastasis.

Simvastatin inhibits inflammation in ischemia-reperfusion injury.

Ischemia/reperfusion (I/R) is associated with leukocyte accumulation and tissue injury. The aim of this research was to investigate the protective effect of simvastatin on hind limb I/R inflammation and tissue damage. Mice were subjected to hind limb ischemic insult for 2 h and were simultaneously administered an intraperitoneal injection of simvastatin (5 mg/kg); this was followed by 36 h of reperfusion. Myeloperoxidase (MPO) levels in the muscles of the hind limb were determined. CXC chemokines and pro-inflammatory cytokines, such as macrophage inflammatory protein (MIP)-2, cytokine-induced neutrophil chemoattractant (KC), interleukin (IL)-6, tumor necrosis factor (TNF)-α, and P-selectin, were assessed using enzyme-linked immunosorbent assay (ELISA). Leukocyte rolling and adhesion in vitro was assessed to indicate leukocyte recruitment at the site of inflammation. Quantitative measurement of skeletal muscle tissue injury was performed. The fluorescent dye level in tissue and serum was used to determine hind limb vascular leakage and tissue edema after I/R. Systemic and differentiated leukocytes were also counted. Simvastatin significantly reduced MIP-2, KC, TNF-α, MPO, IL-6, and P-selectin levels compared to the sham group and I/R plus pretreatment with phosphate-buffered saline (PBS) group (P<0.05). Compared to the sham group and I/R plus PBS group, the I/R plus simvastatin group had attenuated inflammation, vascular leakage, and muscular damage (P<0.05). Simvastatin also significantly inhibited leukocyte rolling and adhesion compared to PBS (P<0.05). Our results suggest that simvastatin may be an effective protectant against tissue injury associated with I/R.