Improving reverse osmosis concentrate treatment and nutrients conversion to Chlorella vulgaris bioenergy assisted with granular activated carbon.

Landfill leachate (LL), especially the reverse osmosis concentrate (ROC), is a societal burden due to high toxicity but may have intrinsic values attributing to copious nutrients and organics. ROC bioremediation by microalgae has attracted much attentions benefiting from its extra advantage of bioenergy production. However, efficient microalgae cultivation with ROC is still a challenging task attributing to notorious ROC characteristics, like high chromaticity and toxicity. To alleviate these negative influences, a technique integrating granular activated carbon (GAC) pretreatment and microalgae bioremediation was proposed, with which nitrogen and phosphorus removal efficiencies achieved 100% along with an optimized microalgal biomass concentration of 1.44 g/L and lipid yield of 482.4 mg/L. Furthermore, a total volumetric energy yield of 33.6 kJ/L was acquired, which was conducive to realize energy valorization. The visualization evidence of three-dimensional fluorescence spectroscopy revealed chromaticity degradation mechanism of ROC as humic acids reduction and transfer to family of soluble microbial by-products. Meanwhile, contributions of GAC adsorption and microalgae assimilation on nutrients removal were analyzed. Together, this work provides a promising method and valuable information for ROC bioremediation with microalgae.

CCR7 promote lymph node metastasis via regulating VEGF-C/D-R3 pathway in lung adenocarcinoma.

Lymph node metastasis is still an important issue in metastatic process of lung adenocarcinoma. C-C chemokine receptor 7 (CCR7) has been proved to be closely associated with the metastasis of lung adenocarcinoma, and the mechanism is poorly understood. In order to investigate the relationship between CCR7 and lymph node metastasis in lung adenocarcinoma, and to explore the role of CCR7 in treating lung adenocarcinoma, 40 clinical specimens were collected to define the relationship between CCR7 and lymph node metastasis in lung adenocarcinoma by immunohistochemistry. The siRNA was used to suppress CCR7 expression in A549 cells. The scratch test, transwell test, qRT-PCR, western blot, flow cytometry and immunofluorescence were used to investigate the lymph node metastasis-related function of CCR7 in vitro. The athymic mice subcutaneous injection was used to research lung adenocarcinoma formation in vivo. Clinical case studies show that higher expression of CCR7 in lung adenocarcinoma tissues was associated with a higher lymph node metastasis. Inhibition of expression of CCR7 can reduce the migration and invasion and suppress the expression of VEGF-C, VEGF-D and VEGF-R3 in vitro and in vivo. Moreover, CCR7 silence also suppressed WNT and p-ERK pathways in vitro. All the results indicate that CCR7 can promote lymph node metastasis in lung adenocarcinoma by regulating VEGF-C/D-R3 pathway. Thus CCR7 is proposed to be a potential prediction for poor prognosis of lung adenocarcinoma, and a therapeutic target for lymph node metastasis.

Catanionic lipid nanosystems improve pharmacokinetics and anti-lung cancer activity of curcumin.

Novel catanionic lipid nanosystems (CLNs) incorporating curcumin (CCM) were developed, and improvements in pharmacokinetics and enhanced anti-lung cancer activity were observed. CCM was present in a lipid matrix surrounded by cationic, anionic and zwitterionic surfactants, forming the core-shell nanosystems. Compared with free CCM, the CCM-CLNs had much higher oral and intravenous bioavailabilities due to enhanced absorption and reduced clearance. The CCM-CLNs exhibited greater cytotoxicity in Lewis lung cancer (LLC) cells, which might have been due to increased antiproliferative, proapoptotic and anti-invasive activities and induction of cell cycle arrest. The CCM-CLNs increased the antitumor efficacy of CCM and decreased the tumor growth rate in tumor-bearing mice. This is the first report of induction of apoptosis in LLC cells by CCM through the PI3K/Akt/FoxO1/Bim signaling pathway. Catanionic lipid nanocarriers show promise for the therapeutic delivery of insoluble anti-tumor drugs.

PC4 induces lymphangiogenesis dependent VEGF-C/VEGF-D/VEGFR-3 axis activation in lung adenocarcinoma.

Human transcriptional positive cofactor 4 (PC4) is a novel marker for diagnosis and treatment of advanced human cancers metastasis. In human lung adenocarcinoma, tumor lymphangiogenesis, an important early event, can promotes lymphatic metastasis, while it has been reported that VEGF-C/VEGF-D/VEGFR-3 axis plays an important role in lymphangiogenesis. The proposed study aims to explore whether PC4 correlates with VEGF-C/VEGF-D/VEGFR-3 axis of lymphangiogenesis in the lymph node metastasis during lung adenocarcinoma. Here, small interfering RNA technique was employed to investigate the relationship of PC4 and the VEGF-C/VEGF-D/VEGFR-3 axis in lung adenocarcinoma cell lines as well as tumor xenografts of mice model. And then mRNA and protein levels of PC4, VEGF-C, VEGF-D and VEGFR-3 were analyzed. Moreover, the correlation between PC4 expression and lymphatic vessel density or the rate of metastatsis in vivo was also revealed. Down-regulating PC4 expression resulted in the lower expression of VEGFC, VEGF-D and VEGFR-3 in mRNA and protein levels, and PC4 expression was significantly related with the factor of VEGF-C/VEGF-D/VEGFR-3 axis expression (P<0.05). Meanwhile, high expression level of PC4 was accompanied by the higher density of tumor lymphatic vessels and the rate of metastatsis in vivo (P<0.05). PC4 expression correlated with the levels of VEGF-C, VEGF-D and VEGFR-3 during the development of lymphangiogenesis and lymphatic metastasis in lung adenocarcinoma in vitro and in vivo, which may be a novel marker in the development of lymphangiogenesis and lymphatic metastasis of tumors.

Sonic hedgehog pathway contributes to gastric cancer cell growth and proliferation.

The Sonic Hedgehog (Shh) signaling pathway is commonly activated in gastrointestinal cancer. However, our understanding of the Shh pathway in gastric cancer remains limited. Here we examined the effects of cyclopamine, a specific inhibitor of the Shh signaling pathway, on cell growth and proliferation in gastric primary cancer cells GAM-016 and the MKN-45 cell line. The results showed that the Shh signaling molecules SHH, PTCH, SMO, GLI1, and GLI2 were intact and activated in both types of cells. Furthermore, we observed that cyclopamine inhibited gastric cancer cell proliferation through cell cycle arrest and apoptosis. An in vivo study using NOD/SCID mouse xenografts demonstrated that cyclopamine significantly prevented tumor growth and development. Our study indicated that Shh signaling pathway could promote gastric cancer cell proliferation and tumor development, and blocking this pathway may be a potential strategy in gastric cancer treatment.