Aggressive cancer cells gain robust tumor vascular mimicry (VM) capability that promotes tumor growth and metastasis. is aberrantly overexpressed in vasculogenic cancer cells and regarded as a master gene of tumor VM. Although microRNAs (miRNAs) play an important role in modulating tumor angiogenesis and cancer metastasis, the miRNA that targets expression in cancer cells to inhibit tumor cell-mediated VM is enigmatic. In this study, we found that miR-27b levels are negatively co-related to expression in ovarian cancer cells and tumor cell-mediated VM, and demonstrated that miR-27b could bind to the 3'-untranslated region (3'UTR) of mRNA. Overexpression of miR-27b in aggressive ovarian cancer cell lines Hey1B and ES2 significantly diminished intracellular expression; convincingly, the inhibitory effect of miR-27b could be reversed by miR-27b specific inhibitor. Intriguingly, miR-27b not only effectively suppressed ovarian cancer cell migration and invasion, but also markedly inhibited formation of ovarian cancer cell-mediated capillary-like structures in vitro and suppressed generation of functional tumor blood vessels in mice. Together, our study suggests that miR-27b functions as a new inhibitor of ovarian cancer cell-mediated VM through suppression of expression, providing a new potential drug candidate for antitumor VM and anti-ovarian cancer therapy.

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Methylmercury (MeHg) is an environmental neurotoxic substance, which can be absorbed by the human body through the digestive tract, and easily cross the blood-brain barrier, causing irreversible damage to the human central nervous system. Reactive oxygen species (ROS) are involved in various ways of intracellular physiological or pathological processes including neuronal apoptosis. The current studies attempted to explore the role of ROS-mediated PARP/AIF apoptosis signal in the process of MeHg inducing human neuroblastoma cells (SH-SY5Y) death. Here, the present studies found that SH-SY5Y cells underwent apoptosis in response to MeHg, which was accompanied by increased the levels of ROS and calcium ion, and the activation of caspase cascades and poly ADP-ribose polymerase (PARP). The decrease in ROS levels significantly reduced the expression of these proteins and the rate of apoptosis. Inhibition of caspase pathway can reduce the rate of apoptosis, but can not prevent the occurrence of apoptosis. Furthermore, inhibition of PARP signaling can significantly reduce the apoptosis rate and the expression of caspase pathway related proteins. Collectively, these results indicated that ROS mediated activation of caspase pathway and PARP /AIF signaling pathway are involved in MeHg induced apoptosis, and there is a certain relationship between the two pathways.

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