A Rhodamine 6G derivative-infiltrated SiO2 inverse opal was used as a fluorescence-enhancing film sensor for the detection of Bi3+ ions.

BackgroundMiR-216b has been reported to be involved in the development of some cancers, however, the role of miR-216b in colorectal cancer (CRC) remains unclear.PurposeThis study aimed to investigate the mechanism underlying miR-216b-induced CRC development.MethodsWe detected the expression of miR-216b in 80 cases of CRC tissues and cell lines, and further analyzed the association between miR-216b and clinical pathological indicators as well as prognosis. In vitro, the miR-216b overexpression cell model was established for further functional assay.ResultsWe demonstrated that miR-216b in CRC tissues and cell lines was markedly decreased compared with corresponding adjacent normal tissues and colonic mucosal epithelial cell line, and was obviously associated with the TNM stage, lymph node metastases, and poor overall survival as well as recurrence-free survival. Furthermore, we found that miR-216b inhibited cell proliferation, cell cycle, migration, and invasion by targeting 3′-UTR of SRPK1. Besides, SRPK1 over-expression reversed miR-216b-inhibited cell proliferation, migration and invasion, while SRPK1 inhibition aggravated these effects.ConclusionsWe identified that miR-216b suppresses colorectal cancer proliferation, migration and invasion by targeting SRPK1, which shed light on how miR-216b functions in CRC pathogenesis.

The expression of miR-126 and serine-arginine protein kinase 1 (SRPK1) are linked to tumor development; nevertheless, its role in tumor growth and invasion of gastric cancer (GC) and the underlying mechanism has not been clarified. Here, the expression and role of miR-126 and SRPK1 was investigated in GC tissues and cells by in-vitro assay, and then targets of miR-126 were identified by dual-luciferase reporter assay. In this study, miR-126 expression was downregulated, and associated with lymph node metastasis and poor prognosis as well as SRPK1 expression. In vitro assay revealed that miR-126 obviously inhibited proliferation and invasive capability of GC cells. Dualluciferase reporter assay showed that miR-126 targets 3'-UTR of SRPK1 and downregulates its expression. Besides, SRPK1 over-expression promoted cell migration and invasion. In conclusion, we identified that miR-126 suppresses tumor growth and metastasis in GC by targeting SRPK1. The expression of miR-126 suggests GC recurrence and metastasis, which shed crucial light on how miR-126 functions in GC pathogenesis.

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The gut microbiota is a large symbiotic community of anaerobic and facultative aerobic bacteria inhabiting the human intestinal tract, and its activities significantly affect human health. Increasing evidence has suggested that the gut microbiome plays an important role in tumor-related immune regulation. In the tumor microenvironment (TME), the gut microbiome and its metabolites affect the differentiation and function of immune cells regulating the immune evasion of tumors. The gut microbiome can indirectly influence individual responses to various classical tumor immunotherapies, including immune checkpoint inhibitor therapy and adoptive immunotherapy. Microbial regulation through antibiotics, prebiotics, and fecal microbiota transplantation (FMT) optimize the composition of the gut microbiome, improving the efficacy of immunotherapy and bringing a new perspective and hope for tumor treatment.