Hierarchical ZnO composed of ultrathin nanosheets as secondary structures were fabricated through a hydrothermal method. Afterwards, hexagonal wurtzite CdS with diameter between 50-100 nm were incorporated on the wurtzite ZnO sheets with the assistance of ultrasonic irradiation. The hybrid ZnO/ CdS samples were intensively investigated by SEM, TEM, HRTEM, XRD, XPS, PL and the UV-Vis absorption spectrum. The photocatalytic trials confirmed that the ZnO/CdS hierarchical heterostructures exhibit improved degradation efficiency compared to pure ZnO sample under natural sunlight. CdS nanoparticles are believed to serve as photo-sensitizers to extend the absorption spectrum to the visible region and the loading amount was also found to play a crucial role in influencing the degradation efficiency. Moreover, the photodegradation kinetics of RhB via using CdS/ZnO as photocatalysts were also systematically discussed. Finally, a mechanism based on this band-gap alignment was proposed to elucidate the efficiency enhancement of the hybrid photocatalysts.

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Background:Epithelial–mesenchymal transition (EMT) and cancer stem cells (CSCs) are considered to be crucial for cancer biology. The purpose of this study was to determine whether EMT directly led to the acquisition of tumour-initiating capacity in breast cancer cell lines.Methods:Epithelial–mesenchymal transition was induced in five breast cancer cell lines and one normal breast cell line by EMT-related cytokine stimulation. Mesenchymal–epithelial transition (MET) was induced by stably overexpressing miR-200c in three mesenchymal-like breast cancer cell lines. Molecular expression and cell function analysis were performed to evaluate the effect of EMT or MET on tumour-initiating capacity and other biological characteristics.Results:The induction of EMT did not enhance tumour-initiating capacity but, instead, conferred a CD44+/CD24−/low phenotype as well as cell proliferation, migration, and resistance to doxorubicin and radiation on breast cancer cell lines. Furthermore, MET did not lead to inhibition or loss of the tumour-initiating capacity in mesenchymal-like breast cancer cell lines, but it markedly attenuated other malignant properties, including proliferation, invasion, and resistance to therapy.Conclusions:Epithelial–mesenchymal transition does not alter tumour-initiating capacity of breast cancer cells but some other biological characteristics. Therefore, EMT and tumour-initiating capacity may not be directly linked in breast cancer cell lines.