In the clinic, predicting metastasis and chemoresistance takes high priority, but has not been well established. This study seeks to investigate whether dynamically monitoring serum microRNAs (miRNAs) can help predict metastasis, chemoresistance, and prognosis of colorectal cancer. Serum miR-155, miR-200c, and miR-210 levels in 15 patients with colon cancer were measured by real-time PCR at different time points post surgery and chemotherapy for 3 years. Significant increases in miR-155, miR-200c, and miR-210 levels were observed in the serum and tumor tissues of colon cancer patients compared to that of healthy subjects. After surgery and chemotherapy, the serum levels of these miRNAs in patients with good prognosis returned to normal levels found in healthy controls during the 3-year follow-up. In patients with recurrence and distant metastasis, serum miR-155, miR-200c, and miR-210 levels remained at an elevated level or became elevated again after a short period of decline. In patients with good response to chemotherapy for metastatic tumors, re-elevation of miR-155 was not significant compared to miR-200c and miR-210. In contrast, miR-155 re-elevated more significantly in patients not sensitized to chemotherapy than miR-200c and miR-210. Our study suggests that re-elevation or sustained elevation of serum miR-155 level after surgery and chemotherapy is a sign of chemoresistance in colon cancer, while high and/or re-elevated miR-155, miR-200c, and miR-210 levels implicate local recurrence and distant metastasis as well as poor prognosis.

The expression of miR-200c has been widely reported to be elevated in tumor tissues and sera of patients with colorectal cancer (CRC) and has been found to correlate with poor prognosis. However, how miR-200c regulates the apoptosis, survival, invasion, metastasis, and tumor growth in colon cancer cells remains to be fully elucidated. This study seeks to further investigate the role of miR-200c in colon cancer development. The expression of miR-200c in tumor and peritumoral tissues of 101 colon cancer patients was measured by real-time PCR. miR-200c expression in HCT-116 and HT-29 colon cancer cells was silenced by adenovirus-carried expression of antisense mRNA against miR-200c. The protein levels of PTEN, p53 Ser(15), PP1, and activated caspase-3 in HCT-116 and HT-29 cells were measured by Western blot. This study demonstrated that the expression of miR-200c was significantly higher in tumor tissues than in peritumoral tissues of colon cancer patients. The elevated miR-200c expression significantly correlated with the TNM stage, lymph node metastasis, and invasion of colon cancer. Silencing miR-200c expression significantly induced cell apoptosis, inhibited long-term survival, invasion, and metastasis, and delayed xenograft tumor growth. Importantly, silencing miR-200c expression sensitized the therapeutic effect of Ara-C (Cytarabine). The effects of silencing miR-200c expression were associated with upregulation of PTEN protein and p53 Ser(15) phosphorylation levels in HCT-116 cells and PTEN protein expression in HT-29 cells. In conclusion, miR-200c functions as an oncogene in colon cancer cells through regulating tumor cell apoptosis, survival, invasion, and metastasis as well as xenograft tumor growth through inhibition of PTEN expression and p53 phosphorylation.

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Biocompatibility and biomechanical stability are two of the main obstacles limiting the effectiveness of vascular scaffolds. To improve the biomechanical stability and biocompatibility of these scaffolds, we created a heparin-nanomodified acellular bovine jugular vein scaffold by alternating linkage of heparin and dihydroxy-iron via self-assembly. Features of the scaffold were evaluated in vitro and in vivo. Heparin was firmly linked to and formed nanoscale coatings around the fibers of the scaffold, and the amount of heparin linked was about 808 ± 86 µg/cm 2 (101 ± 11 USP/cm 2 ) per assembly cycle. The scaffolds showed significantly strengthened biomechanical stability with sustained release of heparin for several weeks in vitro. Importantly, the modified scaffolds showed significantly reduced platelet adhesion, stimulated proliferation of endothelial cells in vitro, and reduced calcification in a subcutaneous implantation rat model in vivo. Heparin nanomodification improves the biocompatibility and biomechanical stability of vascular scaffolds.

Gastric cancer is the second leading cause of cancer mortality, but the molecular mechanisms underlying its progression and metastasis remain unclear. CCR7 and Dicer 1 protein expression in 80 gastric adenocarcinomas and 40 peritumoral tissues were measured by immunohistochemical staining. The expression of let-7a miRNA in serum, tumor tissues, and peritumoral tissues was measured by real-time PCR. The role of let-7a in CCR7 protein expression, migration, and invasion of gastric cancer cells was tested in vitro. Dicer 1 protein expression was found to be significantly reduced, whereas CCR7 protein expression was significantly increased in gastric adenocarcinomas compared to peritumoral tissues. The let-7a miRNA levels in the serum and tumor tissues of gastric adenocarcinoma patients were significantly lower than in the serum of healthy controls and peritumoral tissues, respectively. Dicer 1 protein positively correlated with let-7a miRNA level, but negatively correlated with CCR7 protein level in gastric adenocarcinoma. Negative Dicer 1 protein and let-7a miRNA expression and positive CCR7 protein expression significantly correlated with lymph node metastasis, depth of invasion, high clinical TNM stage, and larger tumor size. Let-7a transfection significantly inhibited CCR7 protein expression, migration, and invasion of MNK-45 cells in vitro. High expression of CCR7 protein and low expression of Dicer 1 protein and let-7a miRNA are significantly associated with the metastasis and progression of gastric cancer. High CCR7 protein expression may be caused by the loss of Dicer 1 protein expression and reduced let-7a miRNA level in gastric cancer. The serum let-7a level might be a marker for the diagnosis of gastric cancer.