On the suppression of cathodic hypochlorite reduction by electrolyte additions of molybdate and chromate ions

The goal of this study was to gain a better understanding of the feasibility of replacing Cr(VI) in the chlorate process by Mo(VI), focusing on the cathode reaction selectivity for hydrogen evolution on steel and titanium in a hypochlorite containing electrolyte. To evaluate the ability of Cr(VI) and Mo(VI) additions to hinder hypochlorite reduction, potential sweep experiments on rotating disc electrodes and cathodic current efficiency (CE) measurements on stationary electrodes were performed. Formed electrode films were investigated with scanning electron microscopy and energy-dispersive X-ray spectroscopy. Cathodic hypochlorite reduction is hindered by the Mo-containing films formed on the cathode surface after Mo(VI) addition to the electrolyte, but much less efficient compared to Cr(VI) addition. Very low levels of Cr(VI), in the mM range, can efficiently suppress hypochlorite reduction on polished titanium and steel. Phosphate does not negatively influence the CE in the presence of Cr(VI) or Mo(VI) but the Mo-containing cathode films become thinner if the electrolyte during the film build-up also contains phosphate. For a RuO2-TiO2 anode polarized in electrolyte with 40 mM Mo(VI), the anode potential increased and increased molybdenum levels were detected on the electrode surfac

Zinc finger protein 468 up-regulation of TFAM contributes to the malignant growth and cisplatin resistance of breast cancer cells

Abstract Background Because of the progress on the diagnosis and treatment for patients with breast cancer (BC), the overall survival of the patients has been improved. However, a number of BC patients cannot benefit from the existing therapeutic strategies as the essential molecular events triggering the development of BC are not well understood. Previous studies have shown that abnormal expression of zinc finger proteins is involved in the development of various malignancies, whereas it remains largely unclear on their significance during the progression of BC. In this study, we aimed to explore the clinical relevance, cellular function and underlying mechanisms of zinc finger protein 468 (ZNF468) in BC. Methods The clinical relevance of ZNF468 and TFAM was analyzed based on TCGA database. Overexpression or knockdown of ZNF468 and TFAM were performed by transfecting the cells with overexpression plasmids and siRNAs, respectively. Overexpression and knockdown efficacy was checked by immunoblotting. CCK-8, colony formation, transwell and apoptosis experiments were conducted to check the cellular function of ZNF468 and TFAM. The content of mtDNA was measured by the indicated assay kit. The effects of cisplatin on BC cells were detected by CCK-8 and colony formation assays. The regulation of ZNF468 on TFAM was analyzed by RT-qPCR, immunoblotting, dual luciferase activity and ChIP-qPCR assays. Results ZNF468 was overexpressed in BC patients and inversely correlated with their prognosis. Based on overexpression and knockdown assays, we found that ectopic expression of ZNF468 was essential for the proliferation, growth and migration of BC cells. The expression of ZNF468 also negatively regulated the sensitivity of BC cells to the treatment of cisplatin. Mechanistically, ZNF468 potentiated the transcription activity of TFAM gene via direct binding on its promoter. Lastly, we demonstrated that ZNF468 up-regulation of TFAM was important for the growth, migration and cisplatin resistance in BC cells. Conclusion Our study indicates that ZNF468 promotes BC cell growth and migration via transcriptional activation of TFAM. ZNF468/TFAM axis can serve as the diagnostic and therapeutic target, as well as the predictor of cisplatin effectiveness in BC patients

Additional file 1 of Zinc finger protein 468 up-regulation of TFAM contributes to the malignant growth and cisplatin resistance of breast cancer cells

Additional file 1: Figure S1. The clinical significance of ZNF468 in different groups of BC patients. (A) Analysis of ZNF468 transcript was conducted in normal tissues and cancer tissues derived from BC patients with different molecular characteristics. *p < 0.05. **p < 0.01. ***p < 0.001. (B–E) Overall survival was analyzed on HER+ (B), LumA (C), LumB (D) and TNBC (E) patients who were divided into ZNF468 high expression and low expression group. The number of the patients and p value were presented in the figure. Figure S2. Original WB results