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As a rising star in the photovoltaic field, perovskite solar cells (PSCs) have attracted extensive attention. However, the industrialization development of PSCs still faces the dual challenges of improving efficiency and stability. Herein, a cage polyamine molecule hexamethylenetetramine (HMTA) as additive is incorporated into the tin oxide electron transport layer (ETL). The introduction of HMTA improves the electron extraction ability of SnO2 and optimizes the energy‐level alignment of function layers. The modification of HMTA also passivates the uncoordinated Pb2+ in the perovskite and reduces the oxygen vacancy defects of SnO2, which alleviate trap‐state density and carrier nonradiative recombination. As a result, the PSC based on the SnO2 ETL modified with HMTA achieves a high power conversion efficiency of 22.37% along with good stability. The research results demonstrate a typical case of using cage polyamines to improve the performance and stability of PSCs.

Background Circular RNAs (circRNAs) represent a class of newly identified transcripts that act as competing endogenous RNAs (ceRNAs) to modulate gene expression by competing for the shared microRNAs (miRNAs) in humans. In this study, we set out to investigate the role of the circRNA-miRNA-mRNA ceRNA network in gastric cancer (GC). Methods A differential analysis on GC-related circRNAs, miRNAs and mRNAs was performed utilizing the R language “limma” package, followed by GO and KEGG enrichment analyses. The Cytoscape visualization software was used to construct the circRNA-miRNA-mRNA ceRNA network. RT-qPCR, Western blot assay, immunohistochemistry, RNA pull down, RIP and dual luciferase gene reporter assay were conducted to verify the expression of the related circRNA, miRNA and mRNA and their interaction in GC tissues and cells. Results The bioinformatics analysis screened 13 circRNAs, 241 miRNAs and 7483 mRNAs related to GC. Ten DEmRNAs (AURKA, BUB1, CCNF, FEN1, FGF2, ITPKB, CDKN1A, TRIP13, KNTC1 and KIT) were identified from the constructed PPI network and module analysis, among which AURKA was the most critical. A circ_0061265-miRNA-885-3p-AURKA ceRNA network was constructed. In vitro cell experiment demonstrated significantly upregulated circ_0061265 and AURKA, but downregulated miR-885-3p in GC. Moreover, circ_0061265 promoted the occurrence of GC by competitively binding to miRNA-885-3p to regulate AURKA expression. Conclusion Our work validated that circ_0061265 may increase AURKA expression by competitively binding to miRNA-885-3p, thereby promoting GC development.

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