The spin polarization strategy regulates heterogeneous catalytic activity performance: from fundamentals to applications.

In recent years, there has been significant attention towards the development of catalysts that exhibit superior performance and environmentally friendly attributes. This surge in interest is driven by the growing demands for energy utilization and storage as well as environmental preservation. Spin polarization plays a crucial role in catalyst design, comprehension of catalytic mechanisms, and reaction control, offering novel insights for the design of highly efficient catalysts. However, there are still some significant research gaps in the current study of spin catalysis. Therefore, it is urgent to understand how spin polarization impacts catalytic reactions to develop superior performance catalysts. Herein, we present a comprehensive summary of the application of spin polarization in catalysis. Firstly, we summarize the fundamental mechanism of spin polarization in catalytic reactions from two aspects of kinetics and thermodynamics. Additionally, we review the regulation mechanism of spin polarization in various catalytic applications and several approaches to modulate spin polarization. Moreover, we discuss the future development of spin polarization in catalysis and propose several potential avenues for further progress. We aim to improve current catalytic systems through implementing a novel and distinctive spin engineering strategy.

MicroRNA­145­5p inhibits osteosarcoma cell proliferation by targeting E2F transcription factor 3.

Osteosarcoma is a common type of bone tumor that primarily occurs in children and young adults. MicroRNA (miRNA/miR) dysregulation is associated with the progression of osteosarcoma; therefore, the aim of the present study was to investigate the biological functions and molecular mechanisms of miR­145­5p in osteosarcoma. The expression of miR­145­5p in osteosarcoma tissues and cell lines was quantified using reverse transcription­quantitative PCR (RT­qPCR). The effect of miR­145­5p on the proliferation of osteosarcoma cells was detected using Cell Counting Kit­8 and colony formation assays, as well as cell cycle distribution analysis. The effect of miR­145­5p on tumor growth was further investigated in vivo using a subcutaneous tumor model in nude mice. The interaction between miR­145­5p and E2F transcription factor 3 (E2F3) was determined using bioinformatics analysis, a luciferase assay, RT­qPCR and western blotting. The results revealed that miR­145­5p expression was decreased in osteosarcoma cell lines and tissues compared with the corresponding normal controls. Increased miR­145­5p expression inhibited the proliferation and colony formation ability of osteosarcoma cells, and induced G1 phase arrest. Furthermore, mice injected with tumor cells overexpressing miR­145­5p exhibited smaller tumors than those in the control group. Further investigation revealed that miR­145­5p binds to and decreases the expression of E2F3. In addition, the mRNA levels of E2F3 were negatively associated with miR­145­5p in osteosarcoma tissues, and increasing E2F3 expression abrogated the inhibitory effects of miR­145­5p on osteosarcoma cells. Collectively, the results obtained in the present study suggest that miR­145­5p may suppress the progression of osteosarcoma, and may serve as a useful biomarker for the diagnosis of osteosarcoma, as well as a therapeutic target.

Suppression of CLEC3A inhibits osteosarcoma cell proliferation and promotes their chemosensitivity through the AKT1/mTOR/HIF1α signaling pathway.

Osteosarcoma (OS) is a primary malignant tumor that occurs in bone, and mainly affects children and adolescents. C­type lectin domain family 3 member A (CLEC3A) is a member of the C­type lectin superfamily, which regulates various biological functions of cells. The present study aimed to identify the effects and related mechanisms of CLEC3A in the proliferation and chemosensitivity of OS cells. The expression of CLEC3A in OS was analyzed using the Gene Expression Omnibus data profile GSE99671, and its expression in OS samples was verified using reverse transcription­quantitative PCR (RT­qPCR) and immunohistochemical staining. The relationship between the expression of CLEC3A and clinical traits in patients with OS was also analyzed, including age, tumor size, TNM stage and lymph node metastasis. Cell Counting Kit­8 assays, colony formation assays and cell cycle distribution analysis were used to determine the roles of CLEC3A in the proliferation and chemosensitivity of OS cells. Finally, RT­qPCR and western blotting were used to demonstrate the relationship between CLEC3A and the AKT1/mTOR/hypoxia­inducible factor 1­α (HIF1α) pathway. Both the mRNA and protein expression levels of CLEC3A were increased in OS tissues compared with adjacent non­tumor tissues, and this was positively associated with TNM stage and lymph node metastasis. The genetic knockdown of CLEC3A with small interfering RNA decreased OS cell proliferation and colony formation, and induced G1 phase arrest, whereas the overexpression of CLEC3A increased OS cell proliferation and colony formation, and alleviated G1 phase arrest. The suppression of CLEC3A also promoted enhanced the chemosensitivity of OS cells to doxorubicin (DOX) and cisplatin (CDDP); it also inhibited the expression of AKT1, mTOR and HIF1α, further to the nuclear localization of HIF1α, and HIF1α target gene expression levels, including VEGF, GLUT1 and MCL1 were also decreased. Furthermore, treatment with the AKT activator SC79 blocked the inhibitory effects of CLEC3A silencing in OS cells. In conclusion, these findings suggested that CLEC3A may function as an oncogene in OS, and that the suppression of CLEC3A may inhibit OS cell proliferation and promote chemosensitivity through the AKT1/mTOR/HIF1α signaling pathway.