Anti-H1FX monoclonal antibody Made to order

Background Cervical cancer (CC) is the 4th most common cancer-related death in gynecological cancer worldwide. It has been reported that many lncRNAs contribute to oncogenesis although the fundamental mechanisms are basically unknown. Here, we aimed to identify a novel lncRNA H1FX-AS1 and explore a ceRNA network in CC oncogenesis and progression. Methods The expression level and the association with the prognosis of H1FX-AS1 in CC patients were analyzed based on Cancer Genome Atlas (TCGA) datasets, and further verified in 50 CC patients. The biological role of H1FX-AS1 was investigated in vitro and in vivo by over-expression of H1FX-AS1 in CC cells; the potential binding sites between H1FX-AS1 and miRNA, between miR-324-3p and DACT1 were predicted by LncBASE and Targetscan respectively, which were further verified by dual-luciferase reporter assay, RNA pull-down and point mutation; the relationship between genes was analyzed by Pearson correlation; the rescue experiments were used to further explore the involved molecular mechanism. Results Lower H1FX-AS1 expression in CC tissues was found to be associated with the poor prognosis of CC patients. Over-expression of H1FX-AS1 inhibited CC cell proliferation, migration and invasion, while induced apoptosis by sponging miR-324-3p to up-regulate the DACT1 expression level. Conclusion A novel lncRNA H1FX-AS1 was identified, which acted as a competing endogenous RNA (ceRNA) of miR-324-3p to inhibit DACT1 mediated CC progression. Therefore, H1FX-AS1 is a new prognostic predictor and targeting the factors in the H1FX-AS1/miR-324-3p/DACT1 axis is the novel potential therapeutic strategy for CC.

The linker histone H1fx is the least characterized member of the H1 family. To investigate the developmental changes of H1fx, we performed an immunohistochemical analysis of its expression pattern from embryos to adult mice. We found that H1fx was highly expressed during gastrulation, and was positive in all embryonic germ layers between E8.5 and E10.5, which mostly overlapped with the expression of the proliferation marker Ki-67. Neural and mesenchyme tissues strongly expressed H1fx at E10.5. H1fx expression began to be restricted at around E12.5. Western blot analysis of brain tissues demonstrated that the total expression level of H1fx gradually decreased with time from E12.5 to adulthood, whereas H1f0 was increased over this period. In adult mice, H1fx was restrictively expressed at the hypothalamus, subventricular zone, subgranular zone, medulla of the adrenal grand, islets of Langerhans, and myenteric plexus. Taken together, these data suggest that H1fx is preferentially expressed in immature embryonic cells and plays some roles in cells with neural properties.