Abnormal metabolism of tumour cells is closely related to the occurrence and development of breast cancer, during which the expression of NF‐E2‐related factor 2 (Nrf2) is of great significance. Metastatic breast cancer is one of the most common causes of cancer death worldwide; however, the molecular mechanism underlying breast cancer metastasis remains unknown. In this study, we found that the overexpression of Nrf2 promoted proliferation and migration of breast cancers cells. Inhibition of Nrf2 and overexpression of Kelch‐like ECH‐associated protein 1 (Keap1) reduced the expression of glucose‐6‐phosphate dehydrogenase (G6PD) and transketolase of pentose phosphate pathway, and overexpression of Nrf2 and knockdown of Keap1 had opposite effects. Our results further showed that the overexpression of Nrf2 promoted the expression of G6PD and Hypoxia‐inducing factor 1α (HIF‐1α) in MCF‐7 and MDA‐MB‐231 cells. Overexpression of Nrf2 up‐regulated the expression of Notch1 via G6PD/HIF‐1α pathway. Notch signalling pathway affected the proliferation of breast cancer by affecting its downstream gene HES‐1, and regulated the migration of breast cancer cells by affecting the expression of EMT pathway. The results suggest that Nrf2 is a potential molecular target for the treatment of breast cancer and targeting Notch1 signalling pathway may provide a promising strategy for the treatment of Nrf2‐driven breast cancer metastasis.

No abstract

In contrast to the large number of suitable electrode materials, thorough comprehension of the electrolyte remains lacking. Meanwhile, safety issues and side reactions in sodium-ion batteries caused by traditional organic liquid electrolytes are more severe than those in lithium-ion batteries due to the higher chemical reactivity of sodium than that of lithium which will result in a more drastic reaction with liquid electrolyte. Therefore, the discovery of an effective electrolyte remains a major challenge, which hinders the further application of SIBs. Solid-state sodiumion batteries (SSIBs) based on solid-state electrolytes (SSEs) have emerged as an attractive choice to solve these problems, avoiding safety concerns, and severe side reactions with the electrodes. [7] However, the insufficient ionic conductivity of SSEs is the main challenge for the further development of SSIBs. During the past years, many kinds of SSEs had been reported including ceramic-based, sulfide-based, and polymer electrolytes. [8][9][10][11] Although ceramic-based solid-state electrolyte have attracted much attention due to their high ionic conductivity at room temperature, harsh synthetic conditions (for instance, more than 1000 °C and 24 h) and poor contact capability with the electrodes are the main obstacles. Sulfide-based SSEs, featuring softness and superior ionic conductivity, are other promising alternatives with the merits of low-temperature process capability and good contact with the electrodes. Nevertheless, the chemical instability of the sulfide-based SSEs in ambient atmosphere is the biggest obstacle to make easily fabricated and low-cost solid-state sodium-ion batteries.Compared to the SSEs mentioned above, polymer-based SSEs demonstrate remarkable advantages such as excellent flexibility and excellent contact with electrodes. When employing polymer-based SSEs in large-scale industrial applications, the following parameters should be considered: 1) Effective ionic conductivity at room temperature or even at low temperature could guarantee the normal function of SSIBs in a wide temperature range and ensure a durable cycle life; 2) Excellent thermal stability could inhibit the incident caused by thermal runaway; 3) A large electrochemical window can ensure the compatibility between polymer-based SSEs and a high voltage cathode, thus increasing the energy density of the SSIBs but without electrochemical

Epigenetic modifications such as histone modifications and cytosine hydroxymethylation are linked to tumorigenesis. Loss of 5-hydroxymethylcytosine (5 hmC) by ten-eleven translocation 1 (TET1) down-regulation facilitates tumor initiation and development. However, the mechanisms by which loss of TET1 knockdown promotes malignancy development remains unclear. Here, we report that TET1 knockdown induced epithelial-mesenchymal transition (EMT) and increased cancer cell growth, migration, and invasion in DLD1 cells. Loss of TET1 increased EZH2 expression and reduced UTX-1 expression, thus increasing histone H3K27 tri-methylation causing repression of the target gene E-cadherin. Ectopic expression of the H3K27 demethylase UTX-1 or EZH2 depletion both impeded EZH2 binding caused a loss of H3K27 methylation at epithelial gene E-cadherin promoter, thereby suppressing EMT and tumor invasion in shTET1 cells. Conversely, UTX-1 depletion and ectopic expression of EZH2 enhanced EMT and tumor metastasis in DLD1 cells. These findings provide insight into the regulation of TET1 and E-cadherin and identify EZH2 as a critical mediator of E-cadherin repression and tumor progression.

A facile wet-chemical method for synthesizing a nano-sized NiFe-PBA compound with excellent electrochemical performance.