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Background Head and neck squamous cell carcinomas (HNSCCs) are the sixth most common cancer worldwide. Growing evidence showed that Melanoma-associated antigen-A11 (MAGE-A11) was abnormally expressed in various malignancies, but MAGE-A11 expression and its biological roles in HNSCC had not been reported in detail. The aim of the study was to investigate the association between MAGE-A11 signatures and clinicopathological features of HNSCC patients and uncover its potential mechanisms in HNSCC patients. Methods In the present study, we analyzed the expression of MAGE-A11 gene and evaluated the impact of MAGE-A11 genes expression on clinical outcome from the Cancer Genome Atlas (TCGA) database. MAGE-A11 expression was assessed in a well-characterized series of HNSCC (N = 75) with long-term follow-up and 10 cases of adjacent non-cancerous tissues, which were diagnosed between 2013 and 2014, by using immunohistochemistry. The correlation between MAGE-A11 expression and clinicopathological factors was analyzed. Kaplan-Meier and Cox regression analyses were used to assess the prognostic significance of MAGE-A11 expression among HNSCC patients. Results The results showed that MAGE-A11 mRNA expression was increased in HNSCC tissues compared to "normal" tissues (P < 10-12). MAGE-A11 protein expression was not correlated with lymph node status, relapse, age, gender, histological grade, differentiation, clinical stage, tumor size, radiotherapy or chemotherapy. The patients with high MAGE-A11 expression had lower 5-year overall survival (OS) rates than those with low MAGE-A11 expression as determined using the Kaplan-Meier method. The univariate and multivariate analyses confirmed that elevated MAGE-A11 was an independent prognostic factor for the OS of HNSCC patients. Conclusion These findings indicate that MAGE-A11 may be a valuable diagnostic or prognostic marker as well as a potential molecular therapy target for HNSCC patients.

Objective Human oral squamous cell carcinoma (OSCC) is a major cause of mortality and morbidity worldwide. There is an urgent need to identify bioactive molecules and potential target genes that could inhibit carcinogenesis for OSCC therapy. Fisetin (3,7,3',4'-tetrahydroxyflavone), a naturally occurring flavonoid, has been previously shown to have anti-proliferative activities in OSCC; however, its molecular mechanism is unknown. Methods Colony formation, cell viability, Boyden chamber, wound healing, and tumor xenograft assays were used to detect the impact of fisetin on OSCC cells in vitro and in vivo. Western blot analysis was used to examine the corresponding protein expression. Results Fisetin treatment significantly inhibited proliferation and promoted apoptosis by repressing PAK4 expression. Moreover, fisetin treatment attenuated cell migration by blocking PAK4 signaling pathways. In addition, the tumor xenograft showed anti-tumor growth effects of fisetin exposure in vivo. Conclusion Fisetin may represent a potential therapeutic strategy for human OSCC by targeting PAK4 signaling pathways.

Atherosclerosis is a potentially life-threatening cardiovascular disease characterized by chronic endothelial inflammation and the formation of atherosclerotic lesions. Circulating ox-LDL is known to induce atherosclerosis by triggering oxidative stress, the expression of inflammatory mediators and adhesion molecules, as well as downregulating the atheroprotective transcriptional factor KLF2. Aloperine is an alkaloid compound isolated from the plant Sophora alopecuroides. Here, we employed various experimental methods to determine the effects of aloperine on ox-LDL-induced markers of atherosclerosis. DHE staining revealed that aloperine may restore the oxidant/antioxidant balance in HUVECs by reducing the level of ROS and rescuing the reduction in NOQ-1 and GCLC induced by ox-LDL. Aloperine treatment reduced ox-LDL-induced expression of IL-6, MCP-1, VCAM-1, and E-selectin and rescued the reduction in KLF2. Aloperine also downregulated ox-LDL-induced expression of the LOX-1. We also demonstrate that aloperine improved cell viability and inhibited the adhesion of U937 monocytes to HUVECs. Finally, we demonstrate that the effects of aloperine are mediated through the rescue of KLF2 expression via suppression of the phosphorylation of p53 protein. Together, our results implicate the potential of aloperine as a safe and effective antiatherosclerosis treatment.