Aqueous extract obtained from Mikania micrantha (MMAE) is commonly used as traditional medicine in some countries. We hypothesized that MMAE may inhibit tumor cell growth, both in an in vitro and in vivo setting. In in vitro experiments, two kinds of human cancer cell lines, K562 and Hela were used to test the anti-tumor activity. Inhibitory concentrations (IC50) were obtained from the inhibition curves fitted by regression analysis, inhibitory rates (%) were calculated by MTT assay, morphological changes were observed by transmission electron microscope (TEM), cell cycles were analyzed by flow cytometry (FCM), and DNA ladders were determined by agarose gel electrophoresis. The in vivo anti-tumor activity was evaluated by calculating the tumor inhibitory rates, thymus index and spleen index of S180-bearing mice. Paraffin-embedded sections were used to test the pathologic changes. The result displayed that the growth of K562 and Hela were enhanced when treated with MMAE at 20 μg/mL after 48 h. Other concentrations of MMAE (50, 100, 200, 400 μg/mL) inhibited the proliferation of both kinds of cells. The IC50 values of K562 and Hela at 48 h were 167.16 and 196.27 μg/mL and at 72 h 98.07 and 131.56 μg/mL, respectively. The effects showed time-dose dependence. MMAE led to damages of organelles and induced apoptosis. These results were confirmed by ladder DNA fragmentation profile. MMAE also increased the percentage of cells in G2/M phase and decreased the percentage of cells undergoing G0/G1 and S phase in in vivo tests using S180 cells. MMAE showed antitummor activity in vivo, with its tumor inhibitory rate ranging from 12.1 to 46.9 %. MMAE also induced necrosis, as shown by pathological examination of Hematoxilin-Eosin stained tumor sections. Meanwhile, compared with the control group, the changes of thymus index and spleen index in MMAE treated group were not obvious. This study suggests that MMAE may be an effective agent for cancer therapy with low toxicity.

Electric vehicles (EVs) have great potential for solving problems that threaten sustainability. However, the market penetration of EVs is difficult and slow. From the perspective of consumer resistance, this study proposes a theoretical model to investigate the impacts of two growing personal values in the Chinese context (materialism and ecological consciousness) on consumers’ purchase intention of EVs. The research model was empirically examined with online survey data from 511 general Chinese consumers. The results indicate that consumer resistance is a crucial element hindering EV consumption and that materialism will promote consumer resistance by exerting a positive impact on perceived costs and a negative impact on perceived benefits of purchasing EVs, while ecological consciousness can effectively prevent consumers from developing a resistant attitude by increasing perceived benefits and decreasing perceived costs of purchasing EVs. Furthermore, the mediation tests suggest that value perceptions (perceived costs and perceived benefits) fully mediate the effects of materialism and ecological consciousness on consumer resistance and that resistant attitude fully mediates the relationships between value perceptions and purchase intention of EVs. Theoretically, this study contributes to the literature by investigating the influence of materialism and ecological consciousness of EV consumption and verifying the underlying mechanism linking them. Practically, the findings of this study can provide valuable insights for promoting the market penetration of EVs.

Background: Colorectal cancer (CRC) is one of the most common aggressive malignancies. KLHL22 functions as a tumor suppressor, and previous findings have demonstrated that KLHL22 can regulate the development of breast cancer and CRC. However, few studies have investigated the role of KLHL22 in CRC cell epithelial-to-mesenchymal transition (EMT) and proliferation. The current study aimed to detect the role of KLHL22 in CRC cell proliferation and EMT and to elucidate the probable molecular mechanisms through which KLHL22 is involved with these processes. Materials and Methods: Transwell invasion, MTT, immunohistochemistry and Western blotting assays were performed to evaluate the migration, invasion and proliferation abilities of CRC cells, and the levels of active molecules involved in the Wnt/β-catenin signaling pathway were examined through Western blotting analysis. In addition, the in vivo function of KLHL22 was assessed using a tumor xenograft model. Results: KLHL22 expression was weaker in CRC tissues than in nonmalignant tissues and could inhibit cell invasion, migration, and proliferation in vitro. Furthermore, the regulatory effects of KLHL22 on EMT were partially attributed to the Wnt/β-catenin signaling pathway. The in vivo results also showed that KLHL22 modulated CRC tumorigenesis. Conclusion: KLHL22 can regulate the activity of GSK-3β to influence the level of PI3K, and this regulation promotes EMT inhibition partially through the Wnt/β-catenin signaling pathway.

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