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Cu clusters are generally unstable and their cluster nuclei are difficult to be controlled. Even minor adjustments in the synthesis of Cu clusters can easily lead to great changes in their cluster nuclei. In this work, we have successfully utilized triple collaborative ligands to obtain a pair of infinitely extended Cu12 cluster‐based chains (Cu12‐1 and Cu12‐2). They have identical Cu12 metal core structures but slightly different coordinated ligands. Both Cu12‐1 and Cu12‐2 show excellent thermal and ambient stability. However, they exhibit diverse room‐temperature photoluminescence phenomena. Crystalline Cu12‐2 displays red‐shifted photoluminescence (637 nm) compared with Cu12‐1 (624 nm) due to the relatively smaller LUMO‐HOMO gap caused by the substituent effect of electro‐withdrawing F atoms. Meanwhile, the substituent effect has influences on electronic structures and electrostatic potentials, thus leading to differences in photoluminescence intensity, PLQY, and lifetime. Crystalline Cu12‐1 displays more intense room‐temperature photoluminescence, higher PLQY and longer lifetime. This work provides a valuable approach for how to prepare highly stable Cu clusters and precisely control their structures to regulate their properties. [ABSTRACT FROM AUTHOR]

Human bone marrow-derived mesenchymal stem cells (hBMSCs) are promising candidates for stem cell therapy in clinical trials. Applications of hBMSCs in clinical therapy are limited by cellular senescence due to long-term ex vivo expansion. Metformin, an oral hypoglycemic drug for type 2 diabetes, has been shown to have antiaging effects. However, the mechanisms of metformin in antiaging treatment remain controversial. Here, we used D-galactose (D-gal) to establish an appropriate model of senescent hBMSCs to explore the antiaging effects of metformin. Following metformin treatment with a low concentration range, senescence phenotypes induced by D-gal significantly changed, including generation of reactive oxygen species (ROS), loss of mitochondrial membrane potential (MMP), and cell cycle arrest. In contrast, no apparent change was found in unsenescent hBMSCs. Furthermore, the results show that activation of 5 ′ AMP-activated protein kinase (AMPK) by metformin enhances cell autophagy in senescent hBMSCs. These findings suggest that metformin exerts antiaging function within the low concentration range by enhancing autophagy and exhibits potential benefits for clinical stem cell therapy by ameliorating the ex vivo replicative senescence of hBMSCs. [ABSTRACT FROM AUTHOR]

Simple Summary: Multidrug resistance (MDR) is a major cause of breast cancer (BC) chemotherapy failure. Long noncoding RNAs (lncRNAs) have been shown closely related to the chemoresistance of BC. In this work, the mechanisms of lncRNA-mediated MDR in BC were elaborated from eight sections, including apoptosis, autophagy, DNA repair, cell cycle, drug efflux, epithelial-mesenchymal transition, epigenetic modification and the tumor microenvironment. Additionally, we also discuss the clinical significance of lncRNAs, which may be biomarkers for diagnosis, therapy and prognosis. Breast cancer (BC) is a highly heterogeneous disease and presents a great threat to female health worldwide. Chemotherapy is one of the predominant strategies for the treatment of BC; however, multidrug resistance (MDR) has seriously affected or hindered the effect of chemotherapy. Recently, a growing number of studies have indicated that lncRNAs play vital and varied roles in BC chemoresistance, including apoptosis, autophagy, DNA repair, cell cycle, drug efflux, epithelial-mesenchymal transition (EMT), epigenetic modification and the tumor microenvironment (TME). Although thousands of lncRNAs have been implicated in the chemoresistance of BC, a systematic review of their regulatory mechanisms remains to be performed. In this review, we systematically summarized the mechanisms of MDR and the functions of lncRNAs mediated in the chemoresistance of BC from the latest literature. These findings significantly enhance the current understanding of lncRNAs and suggest that they may be promising prognostic biomarkers for BC patients receiving chemotherapy, as well as therapeutic targets to prevent or reverse chemoresistance. [ABSTRACT FROM AUTHOR]