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Aim: Previous studies have indicated that early metastasis is a major cause of mortality in patients with choriocarcinoma. However, what determines whether early metastasis of choriocarcinoma has occurred is unknown. The emerging role of miRNA in regulating cancer development and progression has been recognized. miR‐373 has been shown to play pivotal roles in tumorigenesis and metastasis. However, whether miR‐373 functions to promote choriocarcinoma metastasis is not clear. The purpose of this study is to determine the function of miR‐373‐3p in the progression of this cancer. Methods: In this study, we first compared epithelial–mesenchymal transition (EMT)‐related markers, which were inversely correlated with miR‐373‐3p expression in trophoblast and choriocarcinoma cell lines. Using PCR and Western blot, upregulation of miR‐373‐3p was observed to inhibit EMT progression. Similarly, gain‐ and loss‐of‐function studies revealed that ectopic miR‐373‐3p overexpression inhibited the migration by transwell methods of choriocarcinoma cells. Results: Our results revealed that miR‐373‐3p acted as an EMT inhibitor in JEG‐3 and JAR cells; this was due to its mediation of the transforming growth factor‐β (TGFβ) signaling pathway, which was responsible for EMT. miRNA microarray analysis demonstrated that miR‐373‐3p interacted with the 3′ untranslated region of TGFβR2 mRNA, and then Western blot and dual‐luciferase reporter gene assays verified this interaction. Conclusion: Our findings suggest that miR‐373‐3p upregulation partly accounts for TGFβR2 downregulation and leads to a restraint of EMT and migration. miR‐373‐3p may therefore serve as a valuable potential target in the treatment of choriocarcinoma. [ABSTRACT FROM AUTHOR]

Abstract Background In folklore, some people take the decoction of Calyx seu Fructus Physalis (CSFP) for lowering blood lipids. The present study is designed to evaluate the lipid-lowering activities of CSFP, and search for its pharmacodynamical material. Methods CSFP was extracted by water and 75% ethanol, respectively. The extracts of CSFP for reducing serum lipid levels were evaluated on mouse model of hyperlipidemia. The optimized extract was subjected to the bioactivity-guided fractionation in which the liquid-liquid extraction, collumn chromatography, the in vivo and in vitro models of hyperlipidemia were utilized. The structure of active component was determined by 13 C-NMR and 1H-NMR. Results The 75% ethanol extract of CSFP decreased the serum total cholesterol (TC) and triglyceride (TG) levels in mouse model of hyperlipidemia. Followed a separation process for the 75% ethanol extract of CSFP, the fraction B was proved to be an active fraction for lowering lipid in vivo and in vitro experiments, which could significantly decrease the serum TC and TG levels in mouse model of hyperlipidemia, and remarkably decrease the increase of TG in primary mouse hepatocytes induced by high glucose and the increase of TG in HepG2 cells induced by oleic acid. The fraction B2, isolated from B on bioactivity-guided fractionation, could significantly decrease TG level in HepG2 cells. One compound with the highest content in B2 was isolated and determined as luteolin-7-O-beta-D-glucopyranoside by NMR spectra. It could significantly reduce the TG level in HepG2 cells, and inhibited the accumulation of lipids by oil red O stain. Conclusion Our results demonstrated that the 75% ethanol extract of CSFP could improve in vitro and in vivo lipid accumulation. Luteolin-7-O-beta-D-glucopyranoside might be a leading pharmacodynamical material of CSFP for lowering lipids.

Cardiomyocyte apoptosis is an important process occurred during cardiac ischaemia‐reperfusion injury. Long non‐coding RNAs (lncRNA) participate in the regulation of various cardiac diseases including ischaemic reperfusion (I/R) injury. In this study, we explored the potential role of lncRNA ACART (anti‐cardiomyocyte apoptosis‐related transcript) in cardiomyocyte injury and the underlying mechanism for the first time. We found that ACART was significantly down‐regulated in cardiac tissue of mice subjected to I/R injury or cultured cardiomyocytes treated with hydrogen peroxide (H2O2). Knockdown of ACART led to significant cardiomyocyte injury as indicated by reduced cell viability and increased apoptosis. In contrast, overexpression of ACART enhanced cell viability and reduced apoptosis of cardiomyocytes treated with H2O2. Meanwhile, ACART increased the expression of the B cell lymphoma 2 (Bcl‐2) and suppressed the expression of Bcl‐2‐associated X (Bax) and cytochrome‐C (Cyt‐C). In addition, PPAR‐γ was up‐regulated by ACART and inhibition of PPAR‐γ abolished the regulatory effects of ACART on cell apoptosis and the expression of Bcl‐2, Bax and Cyt‐C under H2O2 treatment. However, the activation of PPAR‐γ reversed the effects of ACART inhibition. The results demonstrate that ACART protects cardiomyocyte injury through modulating the expression of Bcl‐2, Bax and Cyt‐C, which is mediated by PPAR‐γ activation. These findings provide a new understanding of the role of lncRNA ACART in regulation of cardiac I/R injury. [ABSTRACT FROM AUTHOR]

Collectively migrating tumor cells have been recently implicated in enhanced metastasis of epithelial malignancies. In oral squamous cell carcinoma (OSCC), α v integrin is a crucial mediator of multicellular clustering and collective movement in vitro ; however, its contribution to metastatic spread remains to be addressed. According to the emerging therapeutic concept, dissociation of tumor clusters into single cells could significantly suppress metastasis-seeding ability of carcinomas. This study aimed to investigate the anti-OSCC potential of novel endostatin-derived polypeptide PEP06 as a cluster-dissociating therapeutic agent in vitro. Firstly, we found marked enrichment of α v integrin in collectively invading multicellular clusters in human OSCCs. Our study revealed that metastatic progression of OSCC was associated with augmented immunostaining of α v integrin in cancerous lesions. Following PEP06 treatment, cell clustering on fibronectin, migration, multicellular aggregation, anchorage-independent survival and colony formation of OSCC were significantly inhibited. Moreover, PEP06 suppressed α v integrin/FAK/Src signaling in OSCC cells. PEP06-induced loss of active Src and E-cadherin from cell–cell contacts contributed to diminished collective migration of OSCC in vitro. Overall, these results suggest that PEP06 polypeptide 30 inhibiting α v integrin/FAK/Src signaling and disrupting E-cadherin-based intercellular junctions possesses anti-metastatic potential in OSCC by acting as a cluster-dissociating therapeutic agent. PEP06 polypeptide 30, acting as a cluster-dissociating therapeutic agent, possesses the effect of anti-metastatic potential in oral squamous cell carcinoma by inhibiting α v integrin/FAK/Src signaling and disrupting E-cadherin-based intercellular junctions. Image 1 [ABSTRACT FROM AUTHOR]

Acid whey is generated during the manufacture of acidified dairy products, such as soft cheeses, acid casein ingredients and strained yoghurts. Examples of these whey‐based by‐products include Cottage cheese acid whey and Greek yoghurt acid whey. Alkalisation of acid whey at elevated temperatures (60 °C) precipitates calcium phosphate, which can be recovered and used as an ingredient. The novel application of a liquid–solid hydrocyclone in the size classification of calcium phosphate from heated and neutralised acid whey was investigated in this study. Factors influencing hydrocyclone performance were tested, and the technology was integrated into a membrane filtration‐based process for the production of milk mineral powders. [ABSTRACT FROM AUTHOR]