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Pancreatic cancer is a highly lethal malignancy associated with tissues of the pancreas. Early diagnosis and effective treatment are crucial to improving the survival rate of patients with pancreatic cancer. In a previous study, we employed the cell-SELEX strategy to obtain an ssDNA aptamer termed XQ-2d with high binding affinity for pancreatic cancer. Here, we first identify CD71 as the XQ-2d-binding target. We found that knockdown of CD71 abolished the binding of XQ-2d and that the binding affinity of XQ-2d is associated with membrane-bound CD71, rather than total CD71 levels. Competitive analysis revealed that XQ-2d shares the same binding site on CD71 with transferrin (Tf), but not anti-CD71 antibody. We then used a surface energy transfer (SET) nanoruler to measure the distance between the binding sites of XQ-2d and anti-CD71 *

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Oral squamous cell carcinoma (OSCC) is the most frequent oral cancer in the world, accounting for more than 90% of all oral cancer diagnosis. Circular RNAs (circRNAs) are large types of non-coding RNAs, demonstrating a great capacity of regulating the expression of genes. However, most of the functions of circRNAs are still unknown. Recent research revealed that circRNAs could serve as a miRNA-sponge, consequently regulating the expression of target genes indirectly, including oncogenes. In this study, we built an apoptotic model with TNF-α, and then we confirmed a circRNA associated with the apoptosis of OSCC cells, circDOCK1 by comparing the expression profile of circRNAs in an apoptotic model with that in untreated OSCC cells. We ascertained the presence of circDOCK1 with qRT-PCR and circRNA sequencing. The knockdown of the expression of circDOCK1 led to the increase of apoptosis. Utilizing multiple bioinformatics methods, we predicted the interactions among circRNAs, miRNAs and genes, and built the circDOCK1/miR-196a-5p/BIRC3 axis. Both the silencing of circDOCK1 with small interfering RNA and the upregulation of the expression of miR-196a-5p with mimics led OSCC cells to increase apoptosis and decrease BIRC3 formation. We further confirmed this outcome by comparing the expression of circDOCK1, miR-196a-5p and BIRC3 in oral squamous carcinoma tissue with those in para-carcinoma tissue, and examining the expression profile of circRNAs in oral squamous carcinoma tissue and para-carcinoma tissue with microarray. Our results demonstrated that circDOCK1 regulated BIRC3 expression by functioning as a competing endogenous RNA (ceRNA) and participated in the process of OSCC apoptosis. Thus, we propose that circDOCK1 could represent a novel potential biomarker and therapeutic target of OSCC.

A low-cost semiconductor-based photocatalyst using visible light energy has attracted increasing interest for energy generation and environmental remediation. Herein, plasmonic Bi metal was deposited in situ in g-C3N4@Bi2WO6 microspheres via a hydrothermal method. As an electron-conduction bridge, metallic Bi was inserted as the interlayer between g-C3N4 and the surface of Bi2WO6 microspheres to enhance visible light absorption due to the surface plasmon resonance (SPR) effect and facilitate efficient electron-carrier separation. Different characterization techniques, including XRD, SEM, TEM, UV–vis, XPS, photoluminescence, and photocurrent generation, were employed to investigate the morphology and optical properties of the as-prepared samples. The results indicated that the g-C3N4(20%)@Bi@Bi2WO6 microsphere sample exhibited an extraordinary enhanced photocatalytic activity, higher than those of the g-C3N4, Bi2WO6, and g-C3N4(20%)@Bi2WO6 samples. It implies that the heterostructured combination of g-C3N4, metallic Bi, and Bi2WO6 microspheres provided synergistic photocatalytic activity via an efficient electron transfer process. On the basis of the results, a possible photocatalytic mechanism of the as-prepared samples was proposed. The present study demonstrated the feasibility of utilizing low-cost metallic Bi as a substitute for noble metals to design a doped photocatalysis composite with enhanced photocatalytic performance.

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