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Molybdenum sulfide MoS x is considered as attractive hydrogen evolution catalyst since it is free of noble metals and shows a low overvoltage. Especially, amorphous molybdenum sulfide has attracted attention because of its high catalytic activity. However, the catalytic mechanism of the hydrogen evolution reaction is not yet fully understood. Therefore in our study, layers of MoS x were deposited by reactive magnetron sputtering varying the substrate temperature in the range from room temperature (RT) to 500°C. The morphology and structure of the films change significantly as a function of temperature, from an amorphous to a highly textured 2H-MoS 2 phase. The highest catalytic activity was found for amorphous layers deposited at RT showing an overvoltage of 180 mV at a current density of-10 mAcm-2 in a 0.5 M sulfuric acid electrolyte (pH 0.3) after electrochemical activation. As detected by Raman spectroscopy the RT deposited catalyst consists of [Mo 3 S 13 ] 2and [Mo 3 S 12 ] 2entities which are interconnected via [S 2 ] 2and S 2ligands. When sweeping the potential from 0.2 to-0.3 V vs RHE a massive release of sulfur in form of gaseous H 2 S was observed in the first minutes as detected by differential electrochemical mass spectroscopy (DEMS). After electrochemical cycling for 10 min, the chains of these clusters transform into a layer-type MoS 2-x phase. In this transformation process, H 2 S formation gradually vanishes and H 2 evolution becomes dominant. The new phase is considered as a sulfur deficient molybdenum sulfide characterized by a high number of molybdenum atoms located at the edges of nano-sized MoS x islands, which act as catalytically active centers.

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Prostate cancer is one of the most common malignancies in men, and it urgently demands precise interventions that target the signaling pathways implicated in its initiation, progression, and metastasis. The Notch-1 signaling pathway is closely associated with the pathophysiology of prostate cancer. This study investigated the antitumor effects and mechanisms of curcumin, which is a well-known natural compound from curcuminoids, in prostate cancer cells. Viability, proliferation, and migration were analyzed in two prostate cancer cell lines, DU145 and PC3, after curcumin treatment. Whether the Notch-1 signaling pathway is involved in the antitumor effects of curcumin was examined. Curcumin inhibited the survival and proliferation of PC3 and DU145 cells in a dose- and time-dependent manner and inhibited DU145 migration. Curcumin did not affect the expression of Notch-1 or its active product NICD, but it did inhibit the expression of MT1-MMP and MMP2 proteins in DU145 cells. We found that curcumin inhibited the DNA-binding ability of NICD in DU145 cells. In conclusion, curcumin inhibited the survival and metastasis of prostate cancer cells via the Notch-1 signaling pathway.