Seeking for an advanced electrochemiluminescence (ECL) platform is still an active and continuous theme in the ECL-sensing realm. This work outlines a femtomolar-level and highly selective glutathione (GSH) and adenosine triphosphate (ATP) ECL assay strategy using a facile split-type gold nanocluster (AuNC) probe-based ECL platform. The system utilizes GSH as an efficient etching agent to turn on the MnO2/AuNC-based ECL nanoswitch platform. This method successfully achieves an ultrasensitive detection of GSH, which significantly outperformed other sensors. Based on the above excellent results, GSH-related biological assays have been further established by taking ATP as a model. Combined with the high catalytic oxidation ability of DNAzyme, this ECL sensor can realize ATP assay as low as 1.4 fmol without other complicated exonuclease amplification strategies. Thus, we successfully achieved an ultrahigh sensitivity, extremely wide dynamic range, great simplicity, and strong anti-interference detection of ATP. In addition, the actual sample detection for GSH and ATP exhibits satisfactory results. We believe that our proposed high-performance platform will provide more possibilities for the detection of other GSH-related substances and show great prospect in disease diagnosis and biochemical research.
Introduction Cysteine Protease Inhibitor 1 (CST1), a cystatin superfamily protein with the effect on the inhibition of cysteine protease activity, is reported to be involved in the development of many malignancies. MiR-942-5p has been demonstrated its regulatory effects on some malignancies. However, the roles of CST1 and miR-942-5p on esophageal squamous cell carcinoma (ESCC) are still unknown up to now. Methods The expression of CST1 in ESCC tissues was analyzed by TCGA database, immunohistochemistry, and RT-qPCR, respectively. Matrigel-uncoated or-coated transwell assay was used to determine the effect of CST1 on migration and invasion of ESCC cells. Regulatory effect of miR-942-5p on CST1 was detected by dual luciferase assay. Results CST1 was ectopically highly expressed in ESCC tissues, and had the effect on promoting the migration and invasion of ESCC cells by upregulating phosphorylated levels of key effectors including MEK1/2, ERK1/2, and CREB in MEK/ERK/CREB pathway. Dual-luciferase assay results showed that miR-942-5p had a regulatory effect on targeting CST1. Conclusions CST1 plays a carcinogenic role on ESCC, and miR-942-5p can regulate the migration and invasion of ESCC cells by targeting CST1 to downregulate MEK/ERK/CREB signaling pathway, suggesting that miR-942-5p/CST1 axis might be a promising target for diagnosis and treatment of ESCC.
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