BackgroundQuercetin, nature’s most common flavonoid, possesses anticarcinogenic properties against various forms of cancer. The aim of this study was to investigate the effect of quercetin on breast cancer stem cells in the MDA-MB-231 cell line, and to elucidate the possible mechanisms for those effects.Material/MethodsWe evaluated breast cancer stem cell proliferation, clone generation, and mammosphere formation to determine the effect of quercetin treatment on breast cancer stem cells.ResultsIn our study, quercetin suppressed breast cancer stem cell proliferation, self-renewal, and invasiveness. It also lowered the expression levels of proteins related to tumorigenesis and cancer progression, such as aldehyde dehydrogenase 1A1, C-X-C chemokine receptor type 4, mucin 1, and epithelial cell adhesion molecules.ConclusionsThese results indicate that quercetin targets and destroys breast cancer stem cells, making it a potential novel drug in the fight against cancer.

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T riptolide is a natural active compound that has signifi cant neuroprotective properties and shows promising effects in the treatment of A lzheimer's disease (AD).Recent studies have shown that autophagy occurs in AD. In this study, we determined whether autophagy regulated by triptolide ameliorates neuronal death caused by am yloid-Beta 1-42 (Aβ 1-42 ). We examined the effects of triptolide on cell viability, autophagy, apoptosis, and the protein kinase B/mammalian target of the rapamysin/70 kDa ribosomal protein S6 kinase (Akt/mTOR/p70S6K) signaling pathway in PC12 cells. The results indicated that triptolide treatment exhibited a cytoprotective effect against cell injury induced by Aβ 1-42 . Triptolide also reduced apoptosis and enhanced cell survival by decreasing autophagosome accumulation and inducing autophagic degradation. Furthermore, our results also showed that activating the Akt/mTOR/p70S6K mechanism was one reason for the protection of triptolide. Triptolide treatment protected against Aβ 1-42 -induced cytotoxicity by decreasing autophagosome accumulation, and inducing autophagic degradation in PC12 cells. These fi ndings also suggest that the reduction of autophagosome accumulation observed in triptolide-treated cells was Akt/mTOR/ p70S6K pathway dependent. Overall, triptolide exhibits a neuron protective effect and this study provides new insight into AD prevention and treatment.

Protein arginine methyltransferase 5 (PRMT5) is a major type II enzyme responsible for symmetric dimethylation of arginine (SDMA), and plays predominantly roles in human cancers, including in ovarian cancer. However, the exactly roles and underlying mechanisms of PRMT5 contributing to the progression of ovarian cancer mediated by reprogramming cell metabolism remain largely elusive. Here, we report that PRMT5 is highly expressed and correlates with poor survival in ovarian cancer. Knockdown or pharmaceutical inhibition of PRMT5 is sufficient to decrease glycolysis flux, attenuate tumor growth, and enhance the antitumor effect of Taxol. Mechanistically, we find that PRMT5 symmetrically dimethylates alpha‐enolase (ENO1) at arginine 9 to promotes active ENO1 dimer formation, which increases glycolysis flux and accelerates tumor growth. Moreover, PRMT5 signals high glucose to increase the methylation modification of ENO1. Together, our data reveal a novel role of PRMT5 in promoting ovarian cancer growth by controlling glycolysis flux mediated by methylating ENO1, and highlights that PRMT5 may represent a promising therapeutic target for treating ovarian cancer.

Abstract. Decreased arterial compliance is one of the earliest detectable manifestations of adverse structural and functional changes within the vessel wall in hypertension. The proteomic approach is a powerful technique to analyze a complex mixture of proteins in various settings. Physical activity level was negatively associated with blood pressure. Sixteen 4-week-old male spontaneously hypertensive rats (SHR) and 16 Wistar-Kyoto (WKY) rats were randomly divided into four groups: i) SHR exercise group, ii) SHR rest group, iii) WKY exercise group and iv) WKY rest group. In the SHR and WKY exercise groups, rats were treated with a 6-week load-free swimming protocol (1 h/day, 5 days/week). The blood pressure of the rats was tested by the CODA TM2 single non-invasive blood pressure measurement appliance. After the 6-week swimming protocol, the total aorta excluding abdominal aorta was extracted. The proteins were separated by two-dimensional gel electrophoresis and identified via LC-mass spectrometry (MS)/MS. After 6-week load-free swimming, blood pressure decreased in the SHRs. Compared with sedentary SHRs, 11 spots on the 2D-gel showed a significant difference in exercised SHRs. Nine of these were chosen for further identification. There were 5 upregulated proteins (long-chain specific acyl-CoA dehydrogenase, heat shock protein β-1, isocitrate dehydrogenase subunit α, actin, α cardiac muscle 1 preprotein and calmodulin isoform 2) and 4 downregulated proteins (adipocyte-type fatty acid-binding protein, tubulin β-2C chain, 78 kDa glucose-regulated protein precursor and mimecan). Proteomics is an effective method to identify the target proteins of exercise intervention for hypertension. IntroductionHypertension is the most frequent chronic disease in the developed world. It is a multisystemic disease that affects the heart and kidneys among other organs. The overall functional, structural and biochemical alterations in vasculature have been extensively studied during hypertension, but the molecular mechanisms remain unclear. Decreased arterial compliance is one of the earliest detectable manifestations of adverse structural and functional changes within the vessel wall (1). It has been shown that the proteomic approach is a useful technique to analyze a complex mixture of proteins in various settings, usually by combining two-dimensional electrophoresis and mass spectrometry (MS) (2). Bian et al (3) recently analyzed the proteome of aorta from spontaneously hypertensive rats (SHR). They found that SHR showed a significant alteration in the aortic wall protein profile compared with normal rats.Exercise is a key antihypertensive therapy. It is reported that the physical activity level was negatively associated with blood pressure. In addition, the blood pressure can be decreased with long-term physical activity. Blood pressure of SHRs undergoing the physical activity protocol was lower than that of the normal SHRs. The functional and structural alterations in vasculature occurred in hypertensives following exercise t...