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N‐coordinated Ni sites (NiNx) are effective catalysts for the electrochemical reduction of CO2 to CO. In most researches, modulating the coordination environment of Ni atoms is focused on to improve electrochemical CO2 reduction (ECR) performance. However, the influence of the carbon substrate's structure on the intrinsic activity of NiNx is seldom investigated. The highly curved surface of carbon nanotubes (CNT) may provide a unique curvature effect on NiNx. It is found that the Ni residues in CNT can be atomized to form NiNx sites on the surface of CNT (Ni‐N/CNT@covalent triazine framework [CTF]) through high‐temperature pyrolysis, using a soluble CTF nanosheet as N precursor. The π‐conjugated and ultrathin 2D structure of CTF enables closer interfacial contact between CTF and CNT, which avoids the formation of a thick carbon layer to maximize the curvature effect. Theoretical data reveal that the NiN3 configuration may act as a highly active ECR site, and the curvature effect from CNT can further tune the electronic structure of NiN3, thus improving the ECR kinetics. The Ni‐N/CNT@CTF‐based flow‐cell electrolyzer exhibits a jCO of 201 mA cm−2 at −0.9 V with a high FECO of 98%. [ABSTRACT FROM AUTHOR]

Matrix stiffness potently promotes the malignant phenotype in various biological contexts. Therefore, identification of gene expression to participate in mechanical force signals transduced into downstream biochemical signaling will contribute substantially to the advances in nasopharyngeal carcinoma (NPC) treatment. In the present study, we detected that cortactin (CTTN) played an indispensable role in matrix stiffness‐induced cell migration, invasion, and invadopodia formation. Advances in cancer research have highlighted that dysregulated alternative splicing contributes to cancer progression as an oncogenic driver. However, whether WT‐CTTN or splice variants (SV1‐CTTN or SV2‐CTTN) regulate matrix stiffness‐induced malignant phenotype is largely unknown. We proved that alteration of WT‐CTTN expression modulated matrix stiffness‐induced cell migration, invasion, and invadopodia formation. Considering that splicing factors might drive cancer progression through positive feedback loops, we analyzed and showed how the splicing factor PTBP2 and TIA1 modulated the production of WT‐CTTN. Moreover, we determined that high stiffness activated PTBP2 expression. Taken together, our findings showed that the PTBP2‐WT‐CTTN level increases upon stiffening and then promotes cell migration, invasion, and invadopodia formation in NPC. [ABSTRACT FROM AUTHOR]

The large‐scale growth of semiconducting thin films on insulating substrates enables batch fabrication of atomically thin electronic and optoelectronic devices and circuits without film transfer. Here an efficient method to achieve rapid growth of large‐area monolayer MoSe2 films based on spin coating of Mo precursor and assisted by NaCl is reported. Uniform monolayer MoSe2 films up to a few inches in size are obtained within a short growth time of 5 min. The as‐grown monolayer MoSe2 films are of high quality with large grain size (up to 120 µm). Arrays of field‐effect transistors are fabricated from the MoSe2 films through a photolithographic process; the devices exhibit high carrier mobility of ≈27.6 cm2 V–1 s–1 and on/off ratios of ≈105. The findings provide insight into the batch production of uniform thin transition metal dichalcogenide films and promote their large‐scale applications. [ABSTRACT FROM AUTHOR]

A novel material of Ag3PO4–Ag–Bi2WO6 Z‐scheme heterojunction has been successfully synthesised using a simple deposition–precipitation method. In this work, the authors used diverse techniques to characterise the structure, catalytic performance, and morphology of the prepared materials. Meanwhile, the catalytic performance of prepared materials was evaluated by degrading organic pigment. The excellent catalytic performance of the material is according to the collaboration of Ag nanoparticles in the Ag3PO4–Ag–Bi2WO6 heterojunction. Ag nanoparticles enhance the stableness and activeness of the catalyst by acting as a charge transfer bridge between Ag3PO4 and Bi2WO6, which results in improving electron–hole pairs' separation. Compared with pure Bi2WO6 and Ag3PO4–Bi2WO6 materials, Ag3PO4–Ag–Bi2WO6 has higher decomposition effectiveness of methylene blue under the same conditions. The photocatalytic mechanism was put forward and the process of the hole–electron pair's separation is discussed in detail, which is due to the formation of the Z‐scheme heterojunction with Ag nanoparticles acted as a charge transfer bridge. [ABSTRACT FROM AUTHOR]

Cancer tissues consist of cancer cells, surrounding stromal cells and the extracellular matrix. Cancer‐associated fibroblasts (CAF) are one of the key components of stromal cells. CAF have a great impact on the behavior of cancer cells, including proliferation, invasion, metastasis and chemoresistance in many ways. However, the underlying mechanism had not been fully elucidated. In this study, we investigated the role of CAF in cisplatin resistance of lung cancer cells. By using conditioned medium from CAF (CAF‐CM), we found that CAF decreased the sensitivity of lung cancer cells to cisplatin. RNA sequencing results showed that CAF expressed a higher level of Annexin A3 (ANXA3) than normal fibroblasts (NF), and CAF‐CM incubation increased the ANXA3 level in lung cancer cells. Overexpression of ANXA3 in lung cancer cells increased cisplatin resistance and activated c‐jun N‐terminal kinase (JNK), whereas knockdown of ANXA3 increased cisplatin sensitivity. Further study showed that CAF‐CM enhanced cisplatin resistance by inhibiting cisplatin‐induced apoptosis, determined by repression of caspase‐3 and caspase‐8, through activation of the ANXA3/JNK pathway. Conversely, suppression of JNK activation by specific inhibitor retarded the effect of CAF‐CM and ANXA3 on cisplatin sensitivity. Taken together, our study demonstrated that CAF potentiated chemoresistance of lung cancer cells through a novel ANXA3/JNK pathway both in vitro and in vivo, suggesting ANXA3 could be a potential therapeutic target for the treatment of chemoresistant cancer. [ABSTRACT FROM AUTHOR]