The prevalence, composition and CN of periodontopathogens were closely related to the severity of periodontal disease, and the red complex was related to the severity of clinical symptoms of periodontal diseases. The concentration of hBD-2 in gingival crevicular fluid from periodontal disease sites was higher than that in gingival crevicular fluid from healthy sites, which suggests that hBD-2 expression might be up-regulated by periodontopathogens.
ObjectiveThis study aimed to investigate the role of ficolin-2 (FCN2) in the development and course of hepatocellular carcinoma (HCC) and to contribute to the evolution of innovative HCC therapeutics.MethodsOncomine, GEPIA (Gene Expression Profiling Interactive Analysis), TISIDB (Tumor Immune System Interactions and Drug Bank database), UALCAN (University of Alabama at Birmingham Cancer data analysis portal), UCSC (University of California, Santa Cruz), R package, the Kaplan–Meier technique, Cox regression analysis, LinkedOmics, Pearson’s correlation, and a nomogram were used to investigate the prognostic value of FCN2 in HCC. Co-expressed genes were screened. A protein–protein interaction network was created using the STRING database. Finally, immunohistochemistry was performed to establish the expression of FCN2 in HCC tissues. A pan-cancer study centered on HCC-related molecular analysis was also conducted to look for a link between FCN2 and immune infiltration, immune modulators, and chemokine receptors.ResultsIn HCC tissues, the expression of FCN2 was observed to be lower than that in normal tissues. This was connected to the HCC marker alpha-fetoprotein, showing that FCN2 is involved in the development and progression of cancer. FCN2 may act through Staphylococcus aureus infection, lectins, and other pathways. Furthermore, at the immune level, the expression of FCN2 in HCC was associated with some immune cell infiltration, immunomodulators, and chemokine receptors.ConclusionFCN2 may be an immune checkpoint inhibitor for HCC, creating a breakthrough in the treatment of HCC.
Background To construct the lncRNA-miRNA-mRNA axis based on the study of molecular oncology, to explore the role and mechanism of this axis in the occurrence and development of liver cancer, so as to provide a new channel for the treatment of liver cancer. Methods Using public online databases to establish lncRNA-miRNA-mRNA ceRNA regulation network, after which using QPCR and other experimental techniques to verify that this axis is established and the mechanism of participating in the development of liver cancer. Results It can be concluded from database mining that the expressions of hsa-miR-182-5p and ADH4 are negatively correlated in hepatocellular carcinoma, and LINC01018 is also negatively correlated hsa-miR-182-5p-ADH4, indicating that LINC01018, hsa-miR-182-5p and ADH4 are strongly correlated. Constitute the regulatory axis to participate in the occurrence and development tendency of tumors. LINC01018 regulates ADH4 to inhibit LIHC cell growth by inhibiting hsa-miR-182-5p, providing a feasible theoretical basis for the treatment of HCC.The regulatory axis may also regulate the occurrence and development tendency in liver cancer by adjusting the expression levels of key proteins and phosphorylation proteins in GO and KEGG signaling pathways. Conclusions In this study, it was found that LINC01018/hsa-miR-182-5p/ADH4 ceRNA regulatory axis exists in the human body, and this axis has the possibility of becoming an immune checkpoint inhibitor for liver cancer, which is regarded as a new entry point in the diagnosis and therapy of liver cancer.
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